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Marsdenia tenacissima extract induces G_0/G_1 cell cycle arrest in human esophageal carcinoma cells by inhibiting mitogen-activated protein kinase(MAPK) signaling pathway 认领 引用 被引量：38
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作者 FAN Wei SUN Li +6 位作者 ZHOU Jing-Qian ZHANG Cang QIN Song TANG Ying LIU Yang LIN Sen-Sen YUAN Sheng-Tao 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2015年第6期428-437,共10页
Marsdenia tenacissima extract(MTE, trade name: Xiao-Ai-Ping injection) is an extract of a single Chinese plant medicine. It has been used for the treatment of cancer in China for decades, especially for esophageal can... Marsdenia tenacissima extract(MTE, trade name: Xiao-Ai-Ping injection) is an extract of a single Chinese plant medicine. It has been used for the treatment of cancer in China for decades, especially for esophageal cancer and other cancers in the digestive tract. In the present study, the potential mechanism for MTE's activity in esophageal cancer was explored. The effects of MTE on the proliferation of human esophageal cancer cells(KYSE150 and Eca-109) were investigated by the MTT assay, the Brd U(bromodeoxyuridine) incorporation immunofluorescence assay, and flow cytometric analysis. MTE inhibited cell proliferation through inducing G0/G1 cell cycle arrest in KYSE150 and Eca-109. Western blot analysis was employed to determine protein levels in the MTE treated cells. Compared with the control cells, the expression levels of the cell cycle regulatory proteins cyclin D1/D2/D3, cyclin E1, CDK2/4/6(CDK: cyclin dependent kinase), and p-Rb were decreased significantly in the cells treated with MTE at 40 mg·m L-1. In addition, MTE had an inhibitory effect on the MAPK(mitogen-activated protein kinase) signal transduction pathway, including ERK(extracellular signal-regulated kinase), JNK(c-Jun N-terminal kinase), and p38 MAPK. Moreover, MTE showed little additional effects on the regulation of cyclin D1/D3, CDK4/6, and p-Rb when the ERK pathway was already inhibited by the specific ERK inhibitor U0126. In conclusion, these data suggest that MTE inhibits human esophageal cancer cell proliferation through regulation of cell cycle regulatory proteins and the MAPK signaling pathways, which is probably mediated by the inhibition of ERK activation. 展开更多
关键词 Marsdenia tenacissima extract Cell cycle arrest Mitogen-activated protein kinase signaling pathway Human esophageal cancer
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Downregulation of cold-inducible RNA-binding protein activates mitogen-activated protein kinases and impairs spermatoRenic function in mouse testes 认领 引用 被引量：8
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作者 Zhi-Ping Xia Xin-Min Zheng +3 位作者 Hang Zheng Xiao-Jun Liu Gui-Yong Liu Xing-Huan Wang 《Asian Journal of Andrology》 SCIE CAS CSCD 2012年第6期884-889,共6页
Cold-inducible RNA-binding protein （CIRP） is an RNA-binding protein that is expressed in normal testes and downregulated after heat stress caused by cryptorchidism, varicocele or environmental temperatures. The purp... Cold-inducible RNA-binding protein （CIRP） is an RNA-binding protein that is expressed in normal testes and downregulated after heat stress caused by cryptorchidism, varicocele or environmental temperatures. The purpose of this study was to investigate the functions of CIRP in the testes. We employed RNAi technique to knock down the expression of CIRP in the testes, and performed haematoxylin and eosin staining to evaluate morphological changes following knockdown. Germ cell apoptosis was examined by terminal deoxynucleotidal transferase-mediated dUTP nick end labelling （TUNEL） assay, and mitogen-activated protein kinase （MAPK） signalling pathways were investigated by Western blotting to determine the possible mechanism of apoptosis. We found that using siRNA is a feasible and reliable method for knocking down gene expression in the testes. Compared to controls, the mean seminiferous tubule diameter （MSTD） and the thickness of the germ cell layers decreased following siRNA treatment, whereas the percentage of apoptotic seminiferous tubules increased. The p44/p42, p38 and SAPK/JNK MAPK pathways were activated after downregulation of CIRP. In conclusion, we discovered that downregulation of CIRP resulted in increased germ cell apoptosis, possibly viathe activation of the p44/p42, p38 and SAPK/JNK MAPK pathways. 展开更多
关键词 cold-inducible RNA-binding protein （CIRP） mitogen-activated protein kinase （MAPK） siRNA in vivo spermatogenesis heat stress male infertility
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Antagonistic Effects of N-acetylcysteine on Mitogen-activated Protein Kinase Pathway Activation, Oxidative Stress and Inflammatory Responses in Rats with PM2.5 Induced Lung Injuries 认领 引用 被引量：6
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作者 平芬 曹芹 +1 位作者 林桦 韩书芝 《Chinese Medical Sciences Journal》 CAS CSCD 2019年第4期270-276,共7页
Objective To evaluate the antagonistic effects of N-acetylcysteine(NAC)on mitogen-activated protein kinases(MAPK)pathway activation,oxidative stress and inflammatory responses in rats with lung injury induced by fine ... Objective To evaluate the antagonistic effects of N-acetylcysteine(NAC)on mitogen-activated protein kinases(MAPK)pathway activation,oxidative stress and inflammatory responses in rats with lung injury induced by fine particulate matter(PM2.5).Methods Forty eight male Wistar rats were randomly divided into six groups:blank control group(C1),water drip control group(C2),PM2.5 exposed group(P),low-dose NAC treated and PM2.5 exposed group(L),middle-dose NAC treated and PM2.5 exposed group(M),and high-dose NAC treated and PM2.5 exposed group(H).PM2.5 suspension(7.5 mg/kg)was administered tracheally once a week for four times.NAC of 125 mg/kg,250 mg/kg and 500 mg/kg was delivered intragastrically to L,M and H group respectively by gavage(10 ml/kg)for six days before PM2.5 exposure.The histopathological changes and human mucin 5 subtype AC(MUC5AC)content in lung tissue of rats were evaluated.We investigated IL-6 in serum and bronchoalveolar lavage fluid(BALF)by Enzyme-linked immunosorbent assay(ELISA),MUC5AC in lung tissue homogenate by ELISA,glutathione peroxidase(GSH-PX)in serum and BALF by spectrophotometry,and the expression of p-ERK1/2,p-JNK1/2 and p-p38 proteins by Western blot.All the measurements were analyzed and compared statistically.Results Lung tissue of rats exposed to PM2.5 showed histological destruction and increased mucus secretion of bronchial epithelial cells.Rats receiving NAC treatment showed less histological destruction and mucus secretion.Of P,L,M and H group,MUC5AC in lung tissue,IL-6 in serum and BALF were higher than controls(C1 and C2)(all P<0.05),with the highest levels found in the P group and a decreasing trend with increase of NAC dose.The activity of GSH-PX in serum and BALF of PM2.5 exposed rats(P,L,M and H)was lower than that of controls(all P<0.05),with higher activities found in NAC treated rats(L,M,and H),and an increasing trend with increase of NAC dose.The expressions of p-ERK1/2,p-JNK1/2 and p-p38 proteins in PM2.5 exposed lung tissue(P,L,M and H)was higher than controls(all P<0.05),with decreased levels and dose dependent downregulation found in NAC treated rats.Conclusion NAC can antagonize major MAPK pathway activation,lung oxidative stress and inflammatory injury induced by PM2.5 in rats. 展开更多
关键词 fine particulate matter(PM2.5) N-acetylcysteine mitogen-activated protein kinases oxidative stress inflammatory response rats
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Electroacupuncture reduces apoptotic index and inhibits p38 mitogen-activated protein kinase signaling pathway in the hippocampus of rats with cerebral ischemia/reperfusion injury 认领 引用 被引量：19
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作者 Xiao Lan Xin Zhang +3 位作者 Guo-ping Zhou Chun-xiao Wu Chun Li Xiu-hong Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第3期409-416,共8页
Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemiaeperfusion injury.To further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebral... Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemiaeperfusion injury.To further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebral ischemiaeperfusion injury was associated with the p38 mitogen-activated protein kinase（MAPK） signaling pathway.We established rat models of cerebral ischemiaeperfusion injury using the modified Zea-Longa＇s method.At 30 minutes before model establishment,p38 MAPK blocker SB20358 was injected into the left lateral ventricles.At 1.5 hours after model establishment,electroacupuncture was administered at acupoints of Chize（LU5）,Hegu（LI4）,Zusanli（ST36）,and Sanyinjiao（SP6） for 20 minutes in the affected side.Results showed that the combination of EA and SB20358 injection significantly decreased neurologic impairment scores,but no significant differences were determined among different interventional groups.Hematoxylin-eosin staining also showed reduced brain tissue injuries.Compared with the SB20358 group,the cells were regularly arranged,the structures were complete,and the number of viable neurons was higher in the SB20358 ＋ electroacupuncture group.Terminal deoxynucleotidyl transferase（Td T）-mediated d UTP nick-end labeling assay showed a decreased apoptotic index in each group,with a significant decrease in the SB20358 ＋ electroacupuncture group.Immunohistochemistry revealed reduced phosphorylated p38 expression at 3 days in the electroacupuncture group and SB20358 ＋ electroacupuncture group compared with the ischemiaeperfusion group.There was no significant difference in phosphorylated p38 expression between the ischemiaeperfusion group and SB20358 group.These findings confirmed that the electroacupuncture effects on mitigating cerebral ischemiaeperfusion injury are possibly associated with the p38 MAPK signaling pathway.A time period of 3 days could promote the repair of ischemic cerebral nerves. 展开更多
关键词 nerve regeneration brain injury electroacupuncture cell apoptosis cerebral ischemiaeperfusion injury neurological impairment score morphological changes immunohistoehemical assay p38 mitogen-activated protein kinases phosphorylated p38 hippocampus neural regeneration
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Shenfuqiangxin Capsule inhibits apoptosis through mitogen-activated protein kinase signal pathway in rats with cardio-renal syndrome induced by infrarenal aortic-clamping 认领 引用 被引量：3
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作者 Wang Lei Wang Zi +3 位作者 Yuan Ling Hao Di LüNan Li Xu 《Journal of Traditional Chinese Medicine》 SCIE CSCD 2017年第1期80-87,共8页
OBJECTIVE: To investigate the effect of Shenfuqiangxin capsule and the underlying mechanism on cardio-renal syndrome(CRS) in rats induced by infrarenal aortic-clamping after renal ischaemia.METHODS: Male Wistar rats u... OBJECTIVE: To investigate the effect of Shenfuqiangxin capsule and the underlying mechanism on cardio-renal syndrome(CRS) in rats induced by infrarenal aortic-clamping after renal ischaemia.METHODS: Male Wistar rats underwent infrarenal aortic-clamping after renal ischaemia or sham operation. The surviving CRS rats were divided randomly into three groups: CRS group(CRS + 10 m L·kg-1·d-1pure water by gavage), SFQX group(CRS + 13.2 g crude drug·kg- 1·d- 1Shenfuqiangxin by gavage),and handleregionpeptide(HRP)group(CRS+10mg/kg HRP by vein). Sham operation rats were given10 m L·kg-1·d-1pure water. Treatments were given8 weeks after surgery, which lasted for 4 weeks. Therats were detected for heart structure and function by transthoracic echocardiography. PPR m RNA was detected by Reverse Transcription Polymerase Chain Reaction(RT-PCR). To determine whether the mitogen-activated protein kinase(MAPK) signal pathway is included in the heart and kidney protective function of Shenfuqiangxin capsule, MAPK related proteins such as posophorylated C-Jun amino terminal kinase(p-JNK), posophorylated extracellular signal-regulated kinase ?(p-ERK1/2), posophorylated p38(p-p38) were examined by Western Blot.Apoptosis in heart and kidney tissues were detected by d UTP Nick End Labeling staining.RESULTS: Shenfuqiangxin capsule alleviated myocardial apoptosis and inhibited PRR m RNA expression and p-JNK, p-ERK1/2, p-p38 proteins expression in CRS rats.CONCLUSION: All the results suggest that Shenfuqiangxin capsule improves the injured heart and kidney function maybe through inhibition of MAPK response pathway. 展开更多
关键词 Renal ischaemia Cardi-orenal syndrome Shenfuqiangxin capsule Mitogen-activated protein kinases Infrarenal aortic-clamping (Pro) rennin receptor
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Jiawei Wendan decoction affects mitogen-activated protein kinase signal pathway in the hippocampus of depression rats 认领 引用 被引量：2
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作者 Liping Zhang Man Zhang +2 位作者 Li Wu Meng Xia Guangbin Li 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第36期2805-2809,共5页
A previous study from our group showed that Jiawei Wendan decoction inhibits protein expression of interleukin-1β, 2, and 6, as well as plasma neuropeptide Y, P substance and somatostatin in the hippocampus of depres... A previous study from our group showed that Jiawei Wendan decoction inhibits protein expression of interleukin-1β, 2, and 6, as well as plasma neuropeptide Y, P substance and somatostatin in the hippocampus of depression rat models. The present study analyzed the influence of Jiawei Wendan decoction on the mitogen-activated protein kinase signal transduction pathway in the hippocampus. Results demonstrated that Jiawei Wendan decoction effectively upregulated expression of small molecular G proteins, extracellular regulated kinase 1/2, and activated ribosomal S6 kinase protein in the rat hippocampus. In addition, Jiawei Wendan decoction exhibits antidepressant effects similar to fluoxetine. The underlying mechanisms were shown to be dependent on increased mitogen-activated protein kinase signal transduction pathway activity. 展开更多
关键词 depression hippocarn-pus mitogen-activated protein kinase pathway neural regeneration pathogenesis rats spleen stomach
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Bacteroides fragilis enterotoxin upregulates heme oxygenase-1 in dendritic cells via reactive oxygen species-,mitogen-activated protein kinase-,and Nrf2-dependent pathway 认领 引用 被引量：3
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作者 Su Hyuk Ko Jong Ik Jeon +1 位作者 Hyun Ae Woo Jung Mogg Kim 《World Journal of Gastroenterology》 SCIE CAS 2020年第3期291-306,共16页
BACKGROUND Enterotoxigenic Bacteroides fragilis(ETBF)causes colitis and diarrhea,and is considered a candidate pathogen in inflammatory bowel diseases as well as colorectal cancers.These diseases are dependent on ETBF... BACKGROUND Enterotoxigenic Bacteroides fragilis(ETBF)causes colitis and diarrhea,and is considered a candidate pathogen in inflammatory bowel diseases as well as colorectal cancers.These diseases are dependent on ETBF-secreted toxin(BFT).Dendritic cells(DCs)play an important role in directing the nature of adaptive immune responses to bacterial infection and heme oxygenase-1(HO-1)is involved in the regulation of DC function.AIM To investigate the role of BFT in HO-1 expression in DCs.METHODS Murine DCs were generated from specific pathogen-free C57BL/6 and Nrf2−/−knockout mice.DCs were exposed to BFT,after which HO-1 expression and the related signaling factor activation were measured by quantitative RT-PCR,EMSA,fluorescent microscopy,immunoblot,and ELISA.RESULTS HO-1 expression was upregulated in DCs stimulated with BFT.Although BFT activated transcription factors such as NF-κB,AP-1,and Nrf2,activation of NF-κB and AP-1 was not involved in the induction of HO-1 expression in BFT-exposed DCs.Instead,upregulation of HO-1 expression was dependent on Nrf2 activation in DCs.Moreover,HO-1 expression via Nrf2 in DCs was regulated by mitogenactivated protein kinases such as ERK and p38.Furthermore,BFT enhanced the production of reactive oxygen species(ROS)and inhibition of ROS production resulted in a significant decrease of phospho-ERK,phospho-p38,Nrf2,and HO-1 CONCLUSION These results suggest that signaling pathways involving ROS-mediated ERK and p38 mitogen-activated protein kinases-Nrf2 activation in DCs are required for HO-1 induction during exposure to ETBF-produced BFT. 展开更多
关键词 Bacteroides fragilis enterotoxin Dendritic cells Heme oxygenase-1 Mitogen-activated protein kinases Nrf2 Signaling
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Mechanism of Retinoic Acid and Mitogen-activated Protein Kinases Regulating Hyperoxia Lung Injury 认领 引用 被引量：3
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作者 李文斌 常立文 +5 位作者 容志惠 张谦慎 王华 汪鸿 刘春梅 刘伟 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 2006年第2期178-181,共4页
To investigate the protective effect of retinoic acid （RA） on hyperoxic lung injury and the role of RA as a modulator on mitogen-activated protein kinases （MAPKs）, gastation 21 d Sprague- Dawley （SD） fetuses （t... To investigate the protective effect of retinoic acid （RA） on hyperoxic lung injury and the role of RA as a modulator on mitogen-activated protein kinases （MAPKs）, gastation 21 d Sprague- Dawley （SD） fetuses （term = 22 d） were delivered by hysterotomy. Within 12-24 h of birth, premature rat pups were randomly divided into 4 groups （n= 12 each） ： air-exposed control group （group Ⅰ ） ; hyperoxia-exposed group （ group Ⅱ ）, air-exposed plus RA group （group Ⅲ ）, hyperoxia-exposed plus RA group （group Ⅳ）. Group Ⅰ , Ⅲ were kept in room air, and group Ⅱ , Ⅳ were placed in 85 % oxygen. The pups in groups Ⅲ and Ⅳ were intraperitoneally injected with RA （500 μg/kg every day）. All lung tissues of premature rat pups were collected at the 4th day after birth. Terminal transferase d-UTP nick end labeling （TUNEL） staining was used for the detection of cell apoptosis. The expression of PCNA was immunohistochemically detected. Western blot analysis was employed for the determination of phosphorylated and total nonphosphorylated ERKs, JNKs or p38. Our results showed that lungs from the pups exposed to hyperoxia for 4 d exhibited TUNEL-positive nuclei increased markedly throughout the parenchyma （P〈0.01）, and decreased significantly after RA treatment （P〈0.01）. The index of PCNA-positive cells was significantly decreased （P〈0.01）, and was significantly increased by RA treatment （P〈0.01）. The air-space size was significantly enlarged, secondary crests were markedly decreased in hyperoxia-exposed animals. RA treatment improved lung air spaces and secondary crests in air-exposed pups, hut had no effect on hyperoxia-exposure pups. Western blotting showed that the amounts of JNK, p38 and ERK proteins in hyperoxia-exposure or RA-treated lung tissues were same as those in untreated lung tissues （P〈0.05）, whereas activation of these MAPKs was markedly altered by hyperoxia and RA. After hyperoxia exposure, p-ERK1/2, p-JNK1/2 and p-p38 were dramatically increased （P〈0.01）, whereas p-JNK1/2 and p-p38 were markedly declined and p-ERK1/2 was further elevated by RA treatment （P〈0.01）. It is concluded that RA could decrease cell apoptosis and stimulate cell proliferation under hyperoxic condition. The protection Of RA on hyperoxia-induced lung injury was related＇to the regulation of MAP kinase activation. 展开更多
关键词 hyperoxia lung injury mitogen-activated protein kinases retinoic acid apoptosis proliferation
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Involvement of mitogen-activated protein kinase pathways in N-methyl-D-aspartate-induced excitotoxicity 认领 引用 被引量：1
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作者 Xiaorong Yang Ping Sun +5 位作者 Huaping Qin Rui Wang Ye Wang Ruihong Shi Xin Zhao Ce Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第4期288-294,共7页
Previous studies have shown that mitogen-activated protein kinase （MAPK） signaling pathways are involved in N-methyI-D-aspartate （NMDA）-mediated excitotoxicity. However, a systematic observation or analysis of the... Previous studies have shown that mitogen-activated protein kinase （MAPK） signaling pathways are involved in N-methyI-D-aspartate （NMDA）-mediated excitotoxicity. However, a systematic observation or analysis of the role of these various MAPK pathways in excitotoxicity processes does not exist. The present study further evaluated the role and contribution of three MAPK pathways extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 MAPK in an NMDA-mediated excitotoxicity model using MAPK^specific inhibitor. Results demonstrated that c-Jun N-terminal kinase inhibitor SP600125 and/or p38 MAPK inhibitor SB203580 inhibited NMDA-induced reduction in cell viability, as well as reduced NMDA-induced lactate dehydrogenase leakage and reactive oxygen species production. However, PD98059, an inhibitor of extracellular signal-regulated kinase, did not influence this model. Results demonstrated an involvement of c-Jun N-terminal kinase and p38 MAPK, but not extracellular signal-regulated kinase, in NMDA-mediated excitotoxicity in cortical neurons. 展开更多
关键词 cortical neurons excitotoxicity mitogen-activated protein kinase N-methyI-D-aspartate
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Influence of electroacupuncture on mitogen-activated protein kinase signal transduction in a rat model of cerebral ischemia/reperfusion 认领 引用 被引量：1
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作者 Zhongren Li Meihong Shen +1 位作者 Wenmin Niu Xiaoren Xiang 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第30期2362-2366,共5页
Following electroacupuncture at Baihui （DU 20） and Dazhui （DU 14） in a rat model of cerebral ischemiaeperfusion, extracellular-signal-regulated kinase expression in cerebral cortex and corpus striatum, serum gluta... Following electroacupuncture at Baihui （DU 20） and Dazhui （DU 14） in a rat model of cerebral ischemiaeperfusion, extracellular-signal-regulated kinase expression in cerebral cortex and corpus striatum, serum glutathione reductase, glutathione peroxidase activity, and serum glutathione content were elevated, and neurobehavioral scores improved. However, these effects were antagonized by mitogen-activated protein kinase inhibitor PD98059. Results indicated that electroacupuncture reversed free radical chain reactions and oxidative stress injury caused by cerebral ischemiaeperfusion, thereby providing neuroprotection. This process could correlate with the mitogen-activated protein kinase signal transduction pathway. 展开更多
关键词 anti-oxidative stress cerebral ischemiaeperfusion electroacupuncture mitogen-activated protein kinase pathway signal transduction
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Hippocampal activation of c-Jun N-terminal kinase,protein kinase B,and p38 mitogen-activated protein kinase in a chronic stress rat model of depression 认领 引用 被引量：1
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作者 Wei Dai Weidong Li +2 位作者 Jun Lu Yingge A Ya Tu 《Neural Regeneration Research》 SCIE CAS 2010年第19期1486-1490,共5页
Recent studies have shown that varied stress stimuli activate c-Jun N-terminal kinase （JNK）, protein kinase B （Akt）, and p38 mitogen-activated protein kinase （p38） signal transduction pathway, and also regulate ... Recent studies have shown that varied stress stimuli activate c-Jun N-terminal kinase （JNK）, protein kinase B （Akt）, and p38 mitogen-activated protein kinase （p38） signal transduction pathway, and also regulate various apoptotic cascades. JNK and p38 promote apoptosis, but Akt protects against apoptosis, in hippocampal neurons. However, changes in the transduction pathway in different regions of brain tissues in a chronic stress rat model of depression remain poorly understood. Results from this study showed that JNK phosphorylation levels were significantly greater in the stress group hippocampus compared with the control group （P 〈 0.05）. No significant difference in JNK phosphorylation levels was detected in the rat cerebral cortex between stress and control groups, and no significant difference in Akt and p38 phosphorylation levels was detected in the rat hippocampus and cerebral cortex between stress and control groups （P 〉 0.05）. These results suggested that the JNK signal pathway is activated by JNK phosphorylation and participates in pathophysiological changes in rat models of depression. 展开更多
关键词 depression chronic stress phosphorylation stress-activated protein kinase protein kinase B p38 mitogen-activated protein kinase neural regeneration
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Effects of Mitogen-activated Protein Kinase Signal Pathway on Heat Shock Protein 27 Expression in Human Lens Epithelial Cells Exposed to Sodium Salicylate in vitro 认领 引用 被引量：2
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作者 王智 高瑞莹 +2 位作者 黄渝侃 田博 周龑莉 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 2009年第3期377-382,共6页
The roles of mitogen-activated protein kinase （MAPK） signal pathway in sodium salieylate-induced expression of heat shock protein 27 （HSP27） in human lens epithelial cells （HLECs-B3） in vitro were investigated. ... The roles of mitogen-activated protein kinase （MAPK） signal pathway in sodium salieylate-induced expression of heat shock protein 27 （HSP27） in human lens epithelial cells （HLECs-B3） in vitro were investigated. HLECs-B3 were incubated in the fresh media containing sodium salicylate at different concentrations for different durations, and allowed to be recovered in fresh medium without sodium salicylate for different durations with or without pretreatment with p38MAPK inhibitor （SB203580）, ERK1/2 inhibitor （PD98059） and JNK/SAPK inhibitor （SP600125）. The expression of P38MAPK, ERK1/2, JNK/SAPK, phosphorylated P38MAPK, phosphorylated ERK1/2, phosphorylated JNK/SAPK and HSP27 was detected by Western blot. The expression of HSP27 mRNA and protein was detected by RT-PCR and immunohistochemistry respectively. It was found there was only weak expression of HSP27 in normal HLECs. The expression of HSP27 was not detectable in HLECs-B3 that were exposed to sodium salicylate （55 retool/L） for 1-5 h. It was indicated that recovery from sodium salicylate （〉35 mmol/L） significantly increased the synthesis of HSP27. The expression of HSP27 was up-regulated in HLECs-B3 under sodium salicylate recovery for 3 h, reached the peak level for 6 h, and returned to the level of control cells by 24 h. Activation of P38MAPK from sodium salicylate stimulation occurred at 30th rain, and increased significantly at 1st h, then declined and renamed to baseline level at 3rd h under sodium salicylate recovery. Activation of ERK1/2 occurred at 1st h and reached the peak level at 6th h under sodium salicylate recovery. However, JNK/SAPK was inactivated by sodium salicylate. The expression of HSP27 could be down-regulated with the pretreatment of SB203580 and PD98059 jointly. It is concluded that sodium salicylate can induce the expression of HSP27 in HLECs-B3. The effects are mediated, at least in part, through the activation of P38MAPK and ERK1/2 signaling pathway. 展开更多
关键词 sodium salicylate human lens epithelial cells mitogen-activated protein kinase heat shock protein
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Neuroprotective Effects of Raloxifene on Aβ25-35-induced Damages in PC12 Cells via Mitogen-activated Protein Kinase Signaling Pathway 认领 引用 被引量：1
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作者 Xue DAI Jie WU +3 位作者 Xue-ping SUN Li GAO Yu-gui CUI Jia-yin LIU 《Journal of Reproduction and Contraception》 2012年第1期1-16,共16页
Objective To investigate the neuroprotective effects and the mechanism of this protection of raloxifene （RLX）, a selective estrogen receptor modulator.Methods MTT assay and flow cytometry with annexin V-FITC/PI stai... Objective To investigate the neuroprotective effects and the mechanism of this protection of raloxifene （RLX）, a selective estrogen receptor modulator.Methods MTT assay and flow cytometry with annexin V-FITC/PI staining were performed to evaluate the neuroprotective effects of RLX on Aβ25-35-induced toxicity. The potential mechanisms were studied by Western blotting in cultured rat pheochromocytoma cells （PC12 cells）.Results RLX（1 000 nmol/L）, in combination with Aβ25-35 （30 llmol/L）, increased the cell viability （P 〈0.001）, and reduced the number of apoptotic cells （P 〈0.05）. RLX attenuated Aβ25-35-induced loss of △ψm （P 〈0.01）. The changing of △ψm was similar to the variation of apoptosis. PD98059 （inhibitor of ERK1/2） inhibited the effects of RLX on cell viability and phosphorylation of cleaved caspase-9. No significant difference of cell viability or phosphorylation of cleaved caspase-9 had been found when PC12 cells were incubated with SB203580 （inhibitor of p38MAPK） or SP600125 （inhibitor of JNK）. Afl25.35 induced a time-dependent phosphorylation of p38MAPK and JNK. In PC12 cells treated solely with RLX, ERK1/2 was activated （P〈0.01）. In PC12 cells treated with Aβ25-35 and RLX, Aβ2545-induced phosphorylation of p38MAPK and JNK were inhibited （P〈0.01 and P〈0.001, respectively）.Conclusion RLX inhibited Af125.35-induced cell apoptosis by activating the ERK1/2 pathway in PC12 cells. RLX also attenuated Aβ25-35-induced activation of p38MAPK and JNK. The mitochondria pathway Was involved in this inhibitory effect. 展开更多
关键词 raloxifene Aβ25-35 apoptosis MAPK signaling pathway Alzheimer＇s disease mitogen-activated protein kinase （MAPK）
Retinoic Aacid Diminished the Expression of MMP-2 in Hyperoxia-exposed Premature Rat Lung Fibroblasts through Regulating Mitogen-activated Protein Kinases 认领 引用 被引量：1
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作者 李文斌 常立文 +1 位作者 容志惠 刘伟 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 2011年第2期251-257,共7页
This study examined the effects of retinoic acid （RA）, PD98059, SP600125 and SB203580 on the hyperoxia-induced expression and regulation of matrix metalloproteinase-2 （MMP-2） and metalloproteinase-2 （TIMP-2） in ... This study examined the effects of retinoic acid （RA）, PD98059, SP600125 and SB203580 on the hyperoxia-induced expression and regulation of matrix metalloproteinase-2 （MMP-2） and metalloproteinase-2 （TIMP-2） in premature rat lung fibroblasts （LFs）. LFs were exposed to hyperoxia or room air for 12 h in the presence of RA and the kinase inhibitors PD98059 （ERK1/2）, SP600125 （JNK1/2） and SB203580 （p38） respectively. The expression levels of MMP-2 and TIMP-2 mRNA were detected by semi-quantitative reverse transcription polymerase chain reaction （RT-PCR）. MMP-2 activity was measured by zymography. The amount of p-ERK1/2, REK1/2, p-JNK1/2, JNK1/2, p-p38 and p38 was determined by Western blotting. The results showed that： （1） PD98059, SP600125 and SB203580 significantly inhibited p-ERK1/2, p-JNK1/2 and p-p38 respectively in LFs; （2） The expression of MMP-2 mRNA in LFs exposed to hyperoxia was decreased after treatment with RA, SP600125 and SB203580 respectively （P0.01 or 0.05）, but did not change after treatment with PD98059 （P0.05）. Meanwhile, RA, PD98059, SP600125 and SB203580 had no effect on the expression of TIMP-2 mRNA in LFs exposed to room air or hyperoxia （P0.05）; （3） The expression of pro- and active MMP-2 experienced no change after treatment with RA or SP600125 in LFs exposed to room air （P0.05）, but decreased remarkably after hyperoxia （P0.01 or 0.05）. SB203580 inhibited the expression of pro- and active MMP-2 either in room air or under hyperoxia （P0.01）. PD98059 exerted no effect on the expression of pro- and active MMP-2 （P0.05）. It was suggested that RA had a protective effect on hyperoxia-induced lung injury by down-regulating the expression of MMP-2 through decreasing the JNK and p38 activation in hyperoxia. 展开更多
关键词 hyperoxia retinoic acid lung fibroblasts premature rats matrix metalloproteinase-2 mitogen-activated protein kinases
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Expression and functional analyses of the mitogen-activated protein kinase (MPK) cascade genes in response to phytohormones in wheat ( Triticum aestivum L.) 认领 引用
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作者 YAO Su-fei WANG Yan-xia +3 位作者 YANG Tong-ren HAO Lin LU Wen-jing XIAO Kai 《Journal of Integrative Agriculture》 SCIE CAS CSCD 2017年第1期27-35,共9页
Mitogen-activated protein kinase （MPK） cascades consist of a set of kinase types （MPKKKs, MPKKs, MPKs） to establish conserved signal-transducing modules mediating plant growth, development as well as responses to ... Mitogen-activated protein kinase （MPK） cascades consist of a set of kinase types （MPKKKs, MPKKs, MPKs） to establish conserved signal-transducing modules mediating plant growth, development as well as responses to internal and external cues. In this study, the expression patterns of six MPKKK, two MPKK, and 11 MPK genes in wheat in responses to external treatments of phytohormones, including naphthylacetic acid （NAA）, abscisic acid （ABA）, 6-benzyladenine （6-BA）, gibber- ellin （GA3）, salisylic acid （SA）, jasmonic acid （JA）, and ethylene （ETH）, were investigated. Expression analysis revealed that several of the MPK cascade genes are responses to the external phytohormone signaling. Of which, TaMPKKKA;3 is induced by 6-BA and NAA while TaMPK4 repressed by ETH, GA3, SA, and JA; TaMPKKKA, TaMPKKKA;3 and TaMPK1 are down-regulated by ETH and GA3whereas TaMPK9 and TaMPK12 repressed by ETH and JA in addition that TaMPK12 also repressed by GA3; TaMPK12;1 is down-regulated by ABA, GA3 and SA while TaMPK17 repressed by all exogenous phytonormones examined. TaMPK4, a MPK type gene previously characterized to mediate tolerance to phosphate （Pi） deprivation, was functionally evaluated for its role in mediation of responses of plants to exogenous GA3, ETH, SA, and JA. Results indicated that overexpression and antisense expression of TaMPK4 in tobacco dramatically modify the growth of seedlings upon treatments of GA3, SA and JA, in which the overexpressors behaved deteriorated growth feature whereas the seedlings with antisense expression of TaMPK4 exhibited improved seedling phenotype. The growth behaviors in lines overexpressing or antisensely expressing TaMPK4 are closely associated with the biomass and the corresponding hormone-associated parameters. These results demonstrated that TaMPK4 acts as a critical player in mediating the phyto- hormone signaling. Our findings have identified the phytohormone-responsive MPK cascade genes in wheat and provided a connection between the phytohormone-mediated responses and the MPK cascade pathways. 展开更多
关键词 wheat （Triticum aestivum L.） phytohormone mitogen-activated protein kinase （MPK） cascade expression iransgene analysis
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Differential activation of mitogen-activated protein kinases by γ-irradi-ation in IEC-6 cells: Role of intracellular Ca2+ 认领 引用
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作者 周舟 王小华 +5 位作者 Igisu Hideki 林远 楼淑芬 Matsuoka Masato 程天民 余争平 《Journal of Medical Colleges of PLA(China)》 2002年第3期181-187,共7页
Objective: To explore the effects of γ-irradiation on mitogen-activated protein kinases (MAPKs) and role of intracellular calcium in this event in intestinal epithelial cell line 6 (IEC-6 cells). Methods: After cultu... Objective: To explore the effects of γ-irradiation on mitogen-activated protein kinases (MAPKs) and role of intracellular calcium in this event in intestinal epithelial cell line 6 (IEC-6 cells). Methods: After cultured rat IIEC-6 cells with or without the pretreatment of intracellular Ca2+ chelator were exposed to Y-ir-radiation of 6 Gy, the total and phosphorylated MAPKs in the cells were determined with Western blotting and apoptosis was examined with flow cytometry. Activities of Extracellular signal-regulated protein kinase (ERK) and p38 MAPK were determined by using immuoprecipitation followed by Western blotting. Results: In response to γ-irradiation, phosphorylation of ERK was not significantly observed, while the levels of phosphorylated c-Jun NH2-terminal kinase (JNK) and p38 MAPK were increased in 30 min and reached the peak 2 h after exposure to 6 Gy γ-irradiation, though the cell viability was significantly lowered 12 h. On the other hand, no obvious changes were seen in the total protein levels of ERK, JNK and p38 MAPK. Chelation of intracellular Ca2+ almost completely suppressed the JNK and p38 MAPK phosphorylation induced by γ-irradia-tion, but removal of external Ca2+ had no such effect. Activation of p38 MAPK, but not of ERK, was seen to have a correlation with γ-irradiation induced apoptosis. Conclusion: The results suggest that γ-irradiation is a potent activator for JNK and p38 MAPK, and Ca2+ mobilized from intracellular stores plays an important role in the activation of MAPKs and the induction of apoptosis in IEC-6 cells. 展开更多
关键词 r-irradiation extracellular signal-regulated protein kinase c-Jun NH2-terminal kinase mitogen- activated protein kinases p38 MAPK intracellular Ca2+ intestinal epithelial cell line 6
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Overinhibition of Mitogen-Activated Protein Kinase Inducing Tau Hyperphosphorylation 认领 引用
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作者 LIHong-lian CHENJuan LIUShi-jie ZHANGJia-yu WANGQun WANGJian-Zhi 《Wuhan University Journal of Natural Sciences》 EI CAS 2005年第3期607-610,共4页
To reveal the relationship between mitogen-acti-vated protein kinase (MAPK)and tau phosphorylation, we used different concentration of PD98059, an inhibitor of MEK (MAPKkinase), to treat mice neuroblastma (N2a) cell l... To reveal the relationship between mitogen-acti-vated protein kinase (MAPK)and tau phosphorylation, we used different concentration of PD98059, an inhibitor of MEK (MAPKkinase), to treat mice neuroblastma (N2a) cell line for 6 h. It showed that theactivity of MAPKdecreased in a dose-dependent manner. But Western blot and immunofluo-rescence revealed that justwhen the cells were treated with 16 mu mol/L PD98059, tau was hyperphosphorylated at Ser396/ 404 andSerl99/202 sites. We obtained the conclusion that overinhibited MAPK induced tauhyperphosphorylation at Ser396/404 and Serl99/202 sites. 展开更多
关键词 mitogen-activated protein kinase (MAPK) tau Alzheimer's disease
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Mitogen-activated protein kinase phosphatase 1 protects PC12 cells from amyloid beta-induced neurotoxicity 认领 引用 被引量：7
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作者 Yue Gu Lian-Jun Ma +4 位作者 Xiao-Xue Bai Jing Jie Xiu-Fang Zhang Dong Chen Xiao-Ping Li 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第10期1842-1850,共9页
The mitogen-activated protein kinase（MAPK） signaling pathway plays an important role in the regulation of cell growth, proliferation, differentiation, transformation and death. Mitogen-activated protein kinase phosp... The mitogen-activated protein kinase（MAPK） signaling pathway plays an important role in the regulation of cell growth, proliferation, differentiation, transformation and death. Mitogen-activated protein kinase phosphatase 1（MKP1） has an inhibitory effect on the p38 MAPK and JNK pathways, but it is unknown whether it plays a role in Aβ-induced oxidative stress and neuronal inflammation. In this study, PC12 cells were infected with MKP1 sh RNA, MKP1 lentivirus or control lentivirus for 12 hours, and then treated with 0.1, 1, 10 or 100 μM amyloid beta 42（Aβ42）. The cell survival rate was measured using the cell counting kit-8 assay. MKP1, tumor necrosis factor-alpha（TNF-α） and interleukin-1β（IL-1β） m RNA expression levels were analyzed using quantitative real time-polymerase chain reaction. MKP1 and phospho-c-Jun N-terminal kinase（JNK） expression levels were assessed using western blot assay. Reactive oxygen species（ROS） levels were detected using 2′,7′-dichlorofluorescein diacetate. Mitochondrial membrane potential was measured using flow cytometry. Superoxide dismutase activity and malondialdehyde levels were evaluated using the colorimetric method. Lactate dehydrogenase activity was measured using a microplate reader. Caspase-3 expression levels were assessed by enzyme-linked immunosorbent assay. Apoptosis was evaluated using the terminal deoxynucleotidyl transferase d UTP nick end labeling method. MKP1 overexpression inhibited Aβ-induced JNK phosphorylation and the increase in ROS levels. It also suppressed the Aβ-induced increase in TNF-α and IL-1β levels as well as apoptosis in PC12 cells. In contrast, MKP1 knockdown by RNA interference aggravated Aβ-induced oxidative stress, inflammation and cell damage in PC12 cells. Furthermore, the JNK-specific inhibitor SP600125 abolished this effect of MKP1 knockdown on Aβ-induced neurotoxicity. Collectively, these results show that MKP1 mitigates Aβ-induced apoptosis, oxidative stress and neuroinflammation by inhibiting the JNK signaling pathway, thereby playing a neuroprotective role. 展开更多
关键词 nerve regeneration mitogen-activated protein kinase phosphatase 1 c-Jun N-terminal kinase signaling pathway Alzheimer＇s disease neurons dementia apoptosis RNA interference lentivirus inflammation oxidative stress neural regeneration
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“Three Methods and Three Points” regulates p38 mitogen-activated protein kinase in the dorsal horn of the spinal cord in a rat model of sciatic nerve injury 认领 引用 被引量：9
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作者 Xin Guo Tian-yuan Yu +8 位作者 Wong Steven Wen-duan Jia Chi Ma Yan-hong Tao Chao Yang Tao-tao Lv Shuai Wu Meng-qian Lu Jia-li Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第12期2018-2024,共7页
Tuina is a traditional Chinese treatment for sensory disturbances caused by peripheral nerve injury and related diseases. Our previous studies showed that tuina regulates relevant regions and indices of the spinal dor... Tuina is a traditional Chinese treatment for sensory disturbances caused by peripheral nerve injury and related diseases. Our previous studies showed that tuina regulates relevant regions and indices of the spinal dorsal horn using the Dian, Bo, and Rou method in Yinmen（BL37）, Yanglingquan（GB34）, and Weizhong（BL40）. Treatment prevents muscle atrophy, protects spinal cord neurons, and promotes sciatic nerve repair. The mechanisms of action of tuina for treating peripheral nerve injury remain poorly understood. This study established rat models of sciatic nerve injury using the crushing method. Rats received Chinese tuina in accordance with the principle of ＂Three Methods and Three Points,＂ once daily for 20 days. Tuina intervention reduced paw withdrawal latency and improved wet weight of the gastrocnemius muscle, as well as promoting morphological recovery of sciatic nerve fibers, Schwann cells, and axons. The protein expression levels of phospho-p38 mitogen-activated protein kinase, tumor necrosis factor-α, and interleukin-1β also decreased. These findings indicate that ＂Three Methods and Three Points＂ promoted morphological recovery and improved behavior of rats with peripheral nerve injury. 展开更多
关键词 nerve regeneration tuina Three Methods and Three Points phospho-p38 mitogen-activated protein kinase sciatic nerve injury tumor necrosis factor-α interleukin-1β dorsal horn of the spinal cord neural regeneration
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Bone morphogenetic protein 2-induced human dental pulp cell differentiation involves p38 mitogen-activated protein kinase-activated canonical WNT pathway 认领 引用 被引量：16
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作者 Jing Yang Ling Ye +5 位作者 Tian-Qian Hui Dong-Mei Yang Ding-Ming Huang Xue-Dong Zhou Jeremy J Mao Cheng-Lin Wang 《International Journal of Oral Science》 SCIE CAS CSCD 2015年第2期95-102,共8页
Both bone morphogenetic protein 2（BMP2） and the wingless-type MMTV integration site（WNT）/p-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis.Cross-talk between BMP2 ... Both bone morphogenetic protein 2（BMP2） and the wingless-type MMTV integration site（WNT）/p-catenin signalling pathway play important roles in odontoblast differentiation and dentinogenesis.Cross-talk between BMP2 and WNT/p-catenin in osteoblast differentiation and bone formation has been identified.However,the roles and mechanisms of the canonical WNT pathway in the regulation of BMP2 in dental pulp injury and repair remain largely unknown.Here,we demonstrate that BMP2 promotes the differentiation of human dental pulp cells（HDPCs） by activating WNT/p-catenin signalling,which is further mediated by p38mitogen-activated protein kinase（MAPK） in vitro.BMP2 stimulation upregulated the expression of p-catenin in HDPCs,which was abolished by SB203580 but not by Noggin or LDN193189.Furthermore,BMP2 enhanced cell differentiation,which was not fully inhibited by Noggin or LDN193189.Instead,SB203580 partially blocked BMP2-induced p-catenin expression and cell differentiation.Taken together,these data suggest a possible mechanism by which the elevation of p-catenin resulting from BMP2 stimulation is mediated by the p38 MAPK pathway,which sheds light on the molecular mechanisms of BMP2-mediated pulp reparative dentin formation. 展开更多
关键词 dental catenin morphogenetic stimulation canonical inhibited blocked repair activating mitogen
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