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Synergistic anti-hepatoma effect of triptolide and quercetin via coinhibition and interaction with Janus kinase and mammalian target of rapamycin signal pathway 认领 引用 被引量：1
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作者 Hong-Xuan Tong Jia-Le Zhang +3 位作者 Wen-Yi Nie Li-Jie Jiang Jing-Qing Hu Tao Lu 《World Journal of Gastroenterology》 SCIE CAS 2026年第4期91-109,共19页
BACKGROUND Liver carcinoma,as a major global health concern due to its high incidence and mortality rates.Despite advancements in diagnostic and treatment methodologies,outcomes for hepatocellular carcinoma remain uns... BACKGROUND Liver carcinoma,as a major global health concern due to its high incidence and mortality rates.Despite advancements in diagnostic and treatment methodologies,outcomes for hepatocellular carcinoma remain unsatisfactory.In response to these limitations,patients increasingly turn to alternative therapies such as traditional Chinese medicine,which has demonstrated potential in enhancing quality of life and prolonging survival in combination with conventional treatments.Triptolide(TP)and quercetin,as two broad-spectrum antitumor activities,act through multiple mechanisms,and whether the combination of them can provide a synergistic effect to improve the treatment effect.To optimize the dosage combination of TP and quercetin to maximize their therapeutic benefits in treating liver cancer,potentially advancing the field of drug combination therapy.This approach seeks to explore new treatment strategies and elucidate the underlying mechanisms that could lead to improved outcomes for hepatocellular carcinoma patients facing limited effective treatment options.AIM To investigate the synergistic anti-hepatoma effect of TP and quercetin and elucidate the underlying molecular mechanism involving the Janus kinase(JAK)-signal transducer and activator of transcription(STAT)and mammalian target of rapamycin(mTOR)signaling pathways.METHODS The study utilized 5-week-old female BALB/c-nu mice for establishing a liver cancer subcutaneous transplant tumor model.TP and quercetin were administered intraperitoneally over 21 days to evaluate the effectiveness of the combination,with monitoring of tumor growth.IncuCyte Zoom and CompuSyn software were employed to analyze drug effects for different dose combination on cell proliferation and synergy.Various assays such as CCK-8 cell proliferation analysis,plate cell clone formation,cell scratch experiments,Transwell migration and invasion assays,Annexin V-FITC flow cytometry,and western blotting using specific antibodies were employed to assess cell apoptosis,migration,invasion.Then transcriptome analysis was used RNA sequencing to find the potential synergistic mechanisms and proved by western blotting.RESULTS In vivo,the combination therapy significantly slowed down tumor growth compared to the control group,quercetin alone group,and TP alone group.The tumor inhibition rates were 28.91%(quercetin),28.8%(TP),and 59.3%(combination therapy),respectively.The determination of IncuCyte Zoom and CCK-8 confirmed that there is a concentration gradient and time gradient effect on tumor inhibition,with the synergistic effect of 25 nmol/L TP and 100μmol/L quercetin being the best.Platelet cell clone formation and cell wound scratch assay showed that the combination group had better inhibitory effects.Transwell analysis showed a decrease in migration and invasion in the combination therapy group.Flow cytometry showed that over time,cell apoptosis increased after combination therapy.Transcriptome analysis emphasizes unique pathways influenced by the combination(JAKSTAT and mTOR signaling pathways)and has been validated at the protein level.CONCLUSION Compared with a single drug,the specific metering combination of TP and quercetin has enhanced anti-tumor effects,mediated by inhibition of cell proliferation,inducing cell apoptosis and inhibiting migration/invasion.This synergistic effect is closely related to the simultaneous inhibition of signaling pathways JAK-STAT and mTOR concurrently. 展开更多
关键词 Triptolide Quercetin Synergistic effect Janus kinase signal pathway Mammalian target of rapamycin signal pathway Liver carcinoma
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Bioinformatics-based discovery of the involvement of PSAT1 in mediating the anti-lung adenocarcinoma activity of triptolide 认领 引用
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作者 Zhiwen Cao Lulu Zhang +10 位作者 Wenqiang Zhang Rong Wan Xiaogang Peng Jinyan Xie Ruru Bai Jiejing Jin Changqi Shi Lan Yan Xiangyu Guo Yang Shen Cheng Lu 《Animal Models and Experimental Medicine》 CAS CSCD 2026年第1期115-127,共13页
Background:Triptolide(TP)exhibits various pharmacological activities.Our previous studies have confirmed the efficacy of TP against lung adenocarcinoma(LUAD).However,the potent pharmacological activity of TP is underp... Background:Triptolide(TP)exhibits various pharmacological activities.Our previous studies have confirmed the efficacy of TP against lung adenocarcinoma(LUAD).However,the potent pharmacological activity of TP is underpinned by its complex mechanisms.Exploring its potential mechanisms is of great value for promoting the clinical application of TP and extending its clinical use.Methods:Differentially expressed genes(DEGs)associated with LUAD were analyzed and acquired from the TCGA database,while DEGs related to TP were obtained through RNA sequencing.Hub genes were identified through LASSO and random forest models.The efficacy of TP against LUAD was validated using tumor-bearing mouse models and A549 cells.The validation of hub genes was conducted using RT-qPCR.The regulatory effect of hub genes on TP efficacy was validated through overexpression cell models.Furthermore,the potential mechanisms by which TP improves gemcitabine(GEM)resistance were explored using a GEM-resistant cell line in combination with the overexpression model.Results:This study validated the therapeutic effect of TP against LUAD in vivo and in vitro.Bioinformatics revealed that the mechanism of TP's effect against LUAD might be associated with amino acid-related biological processes.Five hub genes were screened and identified by combining bioinformatics methods and experiments.The overexpression model validated that PSAT1 plays an effective role in the efficacy of TP and in alleviating GEM resistance.Conclusion:This study preliminarily demonstrated that the anti-LUAD effect of TP was associated with the PSAT1-regulated serine biosynthesis pathway,and that TP effectively improves GEM resistance by inhibiting PSAT1 expression. 展开更多
关键词 bioinformatics gemcitabine resistance lung adenocarcinoma PSAT1 triptolide
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Letter to the Editor:Advancing the clinical translation of triptolide and quercetin in hepatocellular carcinoma:A commentary on dual JAK-STAT/mTOR inhibition 认领 引用
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作者 Hua Liu Wei-Yi Jiang Fei-Fei Mao 《World Journal of Gastroenterology》 SCIE CAS 2026年第30期149-153,共5页
Hepatocellular carcinoma(HCC)is a major global health challenge characterized by high incidence and mortality rates.Although the therapeutic landscape for advanced HCC has been revolutionized by the advent of immune c... Hepatocellular carcinoma(HCC)is a major global health challenge characterized by high incidence and mortality rates.Although the therapeutic landscape for advanced HCC has been revolutionized by the advent of immune checkpoint inhibitors and tyrosine kinase inhibitors,many patients exhibit primary or acquired resistance,highlighting the urgent need for novel therapeutic strategies.Combination therapy,the cornerstone of modern HCC management,aims to improve treatment efficacy and overcome resistance by targeting multiple oncogenic pathways simultaneously.Tong et al published a study in the World Journal of Gastroenterology provided insights into the mechanistic synergies underlying these approaches and examined the emerging potential of natural products as sources for novel therapeutic agents.They specifically examined the combination of triptolide and quercetin as a promising strategy that leverages synergistic antitumor effects while mitigating toxicity.This combination co-targets critical signaling networks,including the Janus kinase/signal transducer and activator of transcription and the mammalian target of rapamycin pathways,which play a key role in hepatocarcinogenesis.In this letter,we discuss the main challenges and future directions for translating such preclinical findings into clinical practice,including the need for more relevant preclinical models that incorporate the tumor microenvironment,advanced drug delivery systems to overcome pharmacokinetic limitations,and the identification of predictive biomarkers to guide personalized therapy. 展开更多
关键词 Hepatocellular carcinoma Combination chemotherapy Triptolide Quercetin Janus kinase-signal transducer and activator of transcription pathway Mammalian target of rapamycin pathway
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Targeted Delivery of Triptolide Alleviates Diabetic Nephropathy via Inactivation of JAK2-STAT1 Signaling 认领 引用 被引量：1
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作者 HUANG Rongshuang LI Xinrui +3 位作者 GUO Fan LI Yanping MA Liang FU Ping 《四川大学学报（医学版）》 CAS CSCD 北大核心 2025年第4期907-919,共13页
Objective Inflammation and fibrosis are key features of diabetic nephropathy(DN).Triptolide(TP)exhibits anti-inflammatory and anti-fibrotic properties,though its mechanisms of action in DN remain unclear.CREKA(Cys-Arg... Objective Inflammation and fibrosis are key features of diabetic nephropathy(DN).Triptolide(TP)exhibits anti-inflammatory and anti-fibrotic properties,though its mechanisms of action in DN remain unclear.CREKA(Cys-Arg-Glu-Lys-Ala)is a pentapeptide that specifically binds to fibronectin(FN),and the CREKA-modified liposome(CREKA-Lip)represents a novel FN-targeted drug delivery system.This study aimed to investigate the role of TP in diabetic db/db mice and determine whether encapsulation within CREKA-Lip enhances therapeutic efficacy while reducing the multi-organ toxicity of TP.Methods Eight-week-old diabetic db/db mice received tail vein injections twice weekly with vehicle,free TP,or CREKA-Lip/TP for 10 weeks.Urine and serum parameters were measured,and kidney,heart,liver,and testis tissues were collected for pathological evaluation.Protein-protein interaction networks were constructed using Cytoscape and its plug-ins to identify core targets and elucidate the therapeutic mechanism of TP against DN.Inflammatory,fibrotic,apoptotic,and lipid metabolism markers were evaluated in the kidneys of diabetic mice with DN and in high glucose-treated mouse mesangial cells and podocytes using qPCR,Western blot,immunohistochemistry,and immunofluorescence assays.Results TP administration reduced fasting blood glucose levels and glomerular mesangial expansion in diabetic mice.TP significantly suppressed renal inflammation,fibrosis,and apoptosis while enhancing lipid metabolism.Integration of network pharmacology,molecular docking,and transcriptomics revealed that TP ameliorated DN by inhibiting the JAK2-STAT1 signaling pathway.In vitro,TP inhibited high glucose-induced phosphorylation of JAK2 and STAT1,reduced collagen production in mesangial cells,decreased apoptosis,and improved lipid metabolism in podocytes.Moreover,CREKA-Lip/TP exhibited superior efficacy compared with free TP,with a more sustained reduction in urine albumin-to-creatinine ratio and greater inhibition of mesangial expansion.Notably,CREKA-Lip/TP treatment did not induce systemic toxicity.Conclusion TP improves renal inflammation,fibrosis,apoptosis,and lipid homeostasis,thereby ameliorating DN by inhibiting JAK2-STAT1 activation.Targeted delivery of TP via FN-binding CREKA-Lip enhances therapeutic efficacy while minimizing multi-organ toxicity. 展开更多
关键词 Diabetic nephropathy Triptolide STAT1 Polypeptide-liposome Toxicity
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Increased Alleviation of Bone Destruction in Individuals with Rheumatoid Arthritis via the Coinhibition of the METTL3 and YTHDF1 Axis by the Combination of Triptolide and Medicarpin 认领 引用
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作者 Yi Jiao Zhaoran Wang +11 位作者 Wenya Diao Qishun Geng Xing Wang Xiaoxue Cao Tong Shi Jiahe Xu Lu Zhao Zihan Wang Tiantian Deng Lei Yang Tingting Deng Cheng Xiao 《Engineering》 SCIE EI CSCD 2025年第5期277-291,共15页
Rheumatoid arthritis(RA)is a progressive autoimmune disease characterized by bone destruction that is primarily caused by the overactivation of osteoclasts(OCs),which are critical therapeutic targets.Triptolide(TP)has... Rheumatoid arthritis(RA)is a progressive autoimmune disease characterized by bone destruction that is primarily caused by the overactivation of osteoclasts(OCs),which are critical therapeutic targets.Triptolide(TP)has strong anti-RA effects but is limited by its narrow therapeutic window and associated toxicity,necessitating combination therapy to increase its efficacy and reduce side effects.Medicarpin(Med),a flavonoid with anti-inflammatory and anti-bone destruction properties,has shown potential in reducing osteoclastogenesis.However,the mechanisms underlying the synergistic effects of TP and Med on RA treatment remain unclear.We addressed this issue by evaluating the effects of TP,Med,and their combination on a collagen-induced arthritis(CIA)rat model,with a focus on bone erosion as the primary research endpoint.We subsequently performed experimental validation in an in vitro OC dif-ferentiation model to assess the impacts of these treatments on OC formation and function.Based on polymerase chain reaction(PCR)microarray data from RA patients,further investigations focused on N6-methyladenosine(m6A)methylation and its regulatory factors,methyltransferase-like 3(METTL3)and YT521-B homology domain family protein 1(YTHDF1),which have been identified as potential tar-gets of TP and Med.Key findings revealed that the TP and Med combination significantly alleviated bone destruction and inhibited OC differentiation,exerting stronger effects at lower doses than either drug alone.Mechanistically,TP and Med synergistically modulated METTL3 and YTHDF1 to suppress osteo-clastogenesis through distinct m6 A methylation pathways,contributing to the mitigation of RA-associated bone destruction.Overall,our data highlight the potential of the m6A modification as a ther-apeutic mechanism for the combined use of TP and Med for RA treatment,providing a theoretical basis for the clinical application of herbal active ingredient combinations. 展开更多
关键词 Triptolide Medicarpin Osteoclast Rheumatoid arthritis Methyltransferase-like 3 YT521-B homology domain family protein 1
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Retraction: Triptolide inhibits proliferation and migration of human neuroblastoma SH-SY5Y cells by upregulating microRNA-181a 认领 引用
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作者 Oncology Research Editorial Office 《Oncology Research》 SCIE 2025年第6期1507-1507,共1页
The published article titled“Triptolide inhibits proliferation and migration of human neuroblastoma SH-SY5Y cells by upregulating microRNA-181a”has been retracted from Oncology Research,Vol.26,No.8,2018,PP.1235-1243.
关键词 neuroblastoma microRNA triptolide migration SH SY Y cells proliferation
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16-Hydroxytriptolide" An Active Compound from Tripterygium wilfordii 认领 引用 被引量：1
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作者 马鹏程 吕燮余 +1 位作者 杨晶晶 郑启泰 《Journal of Chinese Pharmaceutical Sciences》 CAS 1992年第2期12-18,共7页
From the dried roots and leaves of Tripterygium wilfordii1.2,a new diter- penoid triepoxide,16-hydroxytriptolide was isolated,and its structure and stereochemistry elucidated as 16-(S)-hydroxy-triptolide on the bas... From the dried roots and leaves of Tripterygium wilfordii1.2,a new diter- penoid triepoxide,16-hydroxytriptolide was isolated,and its structure and stereochemistry elucidated as 16-(S)-hydroxy-triptolide on the basis of spectral data(IR, MS, UV,~1HNMR,13CNMR,2d-NMR,Selective Long-range DEPT)and x-ray crystallographic analysis.This compound showed definite antiinflammatory action,strong immunosuppressive and antifertile activities.In addition,a known compound,triptolide was also isolated and all the spectral signals of^1 HNMR and 13CNMR were assigned. 展开更多
关键词 Tripterygium wilfordii Diterpenoid lactone Diterpenoid epoxide 16-Hy-droxytriptolide Triptolide
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Apoptosis of human pancreatic cancer cells induced by Triptolide 认领 引用 被引量：22
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作者 Guo-Xiong Zhou Xiao-Ling Ding +4 位作者 Jie-Fei Huang Hong Zhang Sheng-Bao Wu Jian-Ping Cheng Qun Wei 《World Journal of Gastroenterology》 SCIE CAS 2008年第10期1504-1509,共6页
AIM:To investigate apoptosis in human pancreatic cancer cells induced by Triptolide(TL),and the relationship between this apoptosis and expression of caspase-3'bcl-2 and bax.METHODS:Human pancreatic cancer cell li... AIM:To investigate apoptosis in human pancreatic cancer cells induced by Triptolide(TL),and the relationship between this apoptosis and expression of caspase-3'bcl-2 and bax.METHODS:Human pancreatic cancer cell line SW1990 was cultured in DMEM media for this study.MTT assay was used to determine the cell growth inhibitory rate in vitro.Flow cytometry and TUNEL assay were used to detect the apoptosis of human pancreatic cancer cells before and after TL treatment.RT-PCR was used to detect the expression of apoptosis-associated gene caspase-3'bcl-2 and bax.RESULTS:TL inhibited the growth of human pancreatic cancer cells in a dose-and time-dependent manner.TL induced human pancreatic cancer cells to undergo apoptosis with typically apoptotic characteristics.TUNEL assay showed that after the treatment of human pancreatic cancer cells with 40 ng/mL TL for 12 h and 24 h,the apoptotic rates of human pancreatic cancer cells increased significantly.RT-PCR demonstrated that caspase-3 and bax were significantly up-regulated in SW1990 cells treated with TL while bcl-2 mRNA was not.CONCLUSION:TL is able to induce the apoptosis in human pancreatic cancer cells.This apoptosis may be mediated by up-regulating the expression of apoptosis-associated caspase-3 and bax gene. 展开更多
关键词 Triptolide Pancreatic cancer Apoptosis Bcl-2 Caspase-3 Bax
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Triptolide Inhibits Expression of Inflammatory Cytokines and Proliferation of Fibroblast-like Synoviocytes Induced by IL-6/sIL-6R-Mediated JAK2/STAT3 Signaling Pathway 认领 引用 被引量：28
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作者 Jian-jing LIN Ke TAO +4 位作者 Nan GAO Hui ZENG De-li WANG Jun YANG Jian WENG 《Current Medical Science》 SCIE CAS 2021年第1期133-139,共7页
Triptolide,a component of the Chinese herb Tripterygium wilfordii Hook F,has been proved to be effective in the treatment of rheumatoid arthritis(RA).However,its underlying mechanisms on RA have not yet been well esta... Triptolide,a component of the Chinese herb Tripterygium wilfordii Hook F,has been proved to be effective in the treatment of rheumatoid arthritis(RA).However,its underlying mechanisms on RA have not yet been well established.We observed the inhibitory effect of triptolide on the expression of inflammatory cytokines and proliferation of fibroblast-like synoviocytes(FLS)induced by the complex of interleukin-6(IL-6)and the soluble form of the IL-6 receptor(sIL-6R).Furthermore,to clarify the underlying mechanisms,we treated FLS with the Janus-activated kinase 2(JAK2)inhibitor/signal transducer and activator of transcription 3(STAT3)activation blocker AZD1480.In this study,immunohistochemical staining was used to identify vimentin(+)and CD68(−)in FLS.The FLS proliferation was measured by cell proliferation assay,and the cell cycles were analyzed by flow cytometry.Furthermore,ELISA was used to detect the expression of the inflammatory factors in culture solution.The expression levels of p-JAK2,JAK2,p-STAT3 and STAT3 were investigated through Western blotting analysis.The results showed that IL-6/sIL-6R significantly increased the cell proliferation and expression of inflammatory cytokines,including IL-6,interleukin-1β(IL-1β)and vascular endothelial growth factor(VEGF).Triptolide or AZD1480 inhibited the cell proliferation and inflammatory cytokine expression in IL-6/sIL-6R-stimulated FLS by suppressing JAK2/STAT3.The study suggested that the physiological effects of triptolide on RA were due to its contribution to the inhibition of the inflammatory cytokine expression and FLS proliferation by suppressing the JAK2/STAT3 signaling pathway.It may provide an innovative insight into the effect of triptolide in preventing RA pathogenesis. 展开更多
关键词 triptolide inflammatory cytokines proliferation fibroblast-like synoviocytes JAK2/STAT3
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Triptolide protects against 1-methyl-4-phenyl pyridinium-induced dopaminergic neurotoxicity in rats:Implication for immunosuppressive therapy in Parkinson’s disease 认领 引用 被引量：28
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作者 高俊鹏 孙珊 +2 位作者 李文伟 陈依萍 蔡定芳 《Neuroscience Bulletin》 CAS 2008年第3期133-142,共10页
Objective Neuroinflammation with microglial activation has been implicated to have a strong association with the progressive dopaminergic neuronal loss in Parkinson＇s disease （PD）. The present study was undertaken ... Objective Neuroinflammation with microglial activation has been implicated to have a strong association with the progressive dopaminergic neuronal loss in Parkinson＇s disease （PD）. The present study was undertaken to evaluate the activation profile of microglia in 1-methyl-4-phenyl pyridinium （MPP^＋）-induced hemiparkinsonian rats. Triptolide, a potent immunosuppressant and microglia inhibitor, was then examined for its efficacy in protecting dopaminergic neurons from injury and ameliorating behavioral disabilities induced by MPP^＋. Methods The rat model of PD was established by intranigral microinjection of MPP^＋. At baseline and on day 1, 3, 7, 14, 21 following MPP^＋ injection, the degree of microglial activation was examined by detecting the immunodensity of OX-42 （microglia marker） in the substantia nigra （SN）. The number of viable dopaminergic neurons was determined by measuring tyrosine hydroxylase （TH） positive neurons in the SN. Behavioral performances were evaluated by counting the number of rotations induced by apomorphine, calculating scores of forelimb akinesia and vibrissae-elicited forelimb placing asymmetry. Results Intranigral injection of MPP^＋ resulted in robust activa- tion of microglia, progressive depletion of dopaminergic neurons, and ongoing aggravation of behavioral disabilities in rats. Triptolide significantly inhibited microglial activation, partially prevented dopaminergic cells from death and improved behavioral performances. Conclusion These data demonstrated for the first time a neuroprotective effect of triptolide on dopaminergic neurons in MPP^＋ induced hemiparkinsonian rats. The protective effect of triptolide may, at least partially, be related to the inhibition of MPP^＋-induced microglial activation. Our results lend strong support to the use of immunosuppressive agents in the management of PD. 展开更多
关键词 Parkinson＇s disease triptolide microglia neurons
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UPLC/ESI-QTOF-MS-based metabolomics survey on the toxicity of triptolide and detoxication of licorice 认领 引用 被引量：10
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作者 WANG Zhuo LIU Jian-Qun +8 位作者 XU Jin-Di ZHU He KONG Ming ZHANG Guo-Hua DUAN Su-Min LI Xiu-Yang LI Guang-Fu LIU Li-Fang LI Song-Lin 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2017年第6期474-480,共7页
Triptolide(TP) from Tripterygium wilfordii has been demonstrated to possess anti-inflammatory, immunosuppressive, and anticancer activities. TP is specially used for the treatment of awkward rheumatoid arthritis, but ... Triptolide(TP) from Tripterygium wilfordii has been demonstrated to possess anti-inflammatory, immunosuppressive, and anticancer activities. TP is specially used for the treatment of awkward rheumatoid arthritis, but its clinical application is confined by intense side effects. It is reported that licorice can obviously reduce the toxicity of TP, but the detailed mechanisms involved have not been comprehensively investigated. The current study aimed to explore metabolomics characteristics of the toxic reaction induced by TP and the intervention effect of licorice water extraction(LWE) against such toxicity. Obtained urine samples from control, TP and TP + LWE treated rats were analyzed by UPLC/ESI-QTOF-MS. The metabolic profiles of the control and the TP group were well differentiated by the principal component analysis and orthogonal partial least squares-discriminant analysis. The toxicity of TP was demonstrated to be evolving along with the exposure time of TP. Eight potential biomarkers related to TP toxicity were successfully identified in urine samples. Furthermore, LWE treatment could attenuate the change in six of the eight identified biomarkers. Functional pathway analysis revealed that the alterations in these metabolites were associated with tryptophan, pantothenic acid, and porphyrin metabolism. Therefore, it was concluded that LWE demonstrated interventional effects on TP toxicity through regulation of tryptophan, pantothenic acid, and porphyrin metabolism pathways, which provided novel insights into the possible mechanisms of TP toxicity as well as the potential therapeutic effects of LWE against such toxicity. 展开更多
关键词 Metabolomics Triptolide Licorice Toxicity Detoxication UPLC/ESI-QTOF-MS
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A pH-sensitive supramolecular nanosystem with chlorin e6 and triptolide co-delivery for chemo-photodynamic combination therapy 认领 引用 被引量：9
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作者 Yihan Wu Jingjing Li +9 位作者 Xuemei Zhong Jinfeng Shi Yanfen Cheng Chenglin He Jiaxin Li Liang Zou Chaomei Fu Meiwan Chen Jinming Zhang Huile Gao 《Asian Journal of Pharmaceutical Sciences》 SCIE CAS 2022年第2期206-218,共13页
The combination of Ce6,an acknowledged photosensitizer,and TPL,a natural anticancer agent,has been demonstrated as a useful strategy to reinforce the tumor growth suppression,as well as decrease the systemic side effe... The combination of Ce6,an acknowledged photosensitizer,and TPL,a natural anticancer agent,has been demonstrated as a useful strategy to reinforce the tumor growth suppression,as well as decrease the systemic side effects compared with their monotherapy.However,in view of the optimal chemo-photodynamic combination efficiency,there is still short of the feasible nanovehicle to steadily co-deliver Ce6 and TPL,and stimuli-responsively burst release drugs in tumor site.Herein,we described the synergistic antitumor performance of a pH-sensitive supramolecular nanosystem,mediated by the host–guest complexing betweenβ-CD and acid pH-responsive amphiphilic co-polymer mPEG-PBAE-mPEG,showing the shell–core structural micelles with the tightβ-CD layer coating.Both Ce6 and TPLwere facilely co-loaded into the spherical supramolecular NPs(TPL+Ce6/NPs)by one-step nanoprecipitation method,with an ideal particle size(156.0 nm),acid pH-responsive drug release profile,and enhanced cellular internalization capacity.In view of the combination benefit of photodynamic therapy and chemotherapy,as well as co-encapsulation in the fabricated pH-sensitive supramolecular NPs,TPL+Ce6/NPs exhibited significant efficacy to suppress cellular proliferation,boost ROS level,lower MMP,and promote cellular apoptosis in vitro.Particularly,fluorescence imaging revealed that TPL+Ce6/NPs preferentially accumulated in the tumor tissue area,with higher intensity than that of free Ce6.As expected,upon 650-nm laser irradiation,TPL+Ce6/NPs exhibited a cascade of amplified synergistic chemo-photodynamic therapeutic benefits to suppress tumor progression in both hepatoma H22 tumor-bearingmice and B16 tumor-bearingmice.More importantly,lower systemic toxicitywas found in the tumor-bearingmice treated with TPL+Ce6/NPs.Overall,the designed supramolecular TPL+Ce6/NPs provided a promising alternative approach for chemo-photodynamic therapy in tumor treatment. 展开更多
关键词 Triptolide Chemo-photodynamic pH-sensitive supramolecular Nanosystem Co-delivery
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Delivery of triptolide with reduction-sensitive polymer nanoparticles for liver cancer therapy on patient-derived xenografts models 认领 引用 被引量：8
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作者 Mengxue He Ling Yu +7 位作者 Yuanyuan Yang Binhua Zou Wen Ma Meng Yu Jiandong Lu Guoliang Xiong Zhiqiang Yu Aimin Li 《Chinese Chemical Letters》 SCIE CAS CSCD 2020年第12期3178-3182,共5页
Hepatocellular carcinoma(HCC)has become the fourth predominant cause of cancer-related deaths worldwide,and HCC is still one of the worst prognoses for survival as it is poorly responsive to both chemotherapy and surg... Hepatocellular carcinoma(HCC)has become the fourth predominant cause of cancer-related deaths worldwide,and HCC is still one of the worst prognoses for survival as it is poorly responsive to both chemotherapy and surgical treatment due to drug resista nce and great toxic effects.Triptolide(TP),a key ingredient from the traditional Chinese medical herb,has been utilized to treat inflammation and antitumor for centuries.However,investigations of this potent agent have been met with only limited success due to the severe systemic toxicities in patients and low water solubility as well as its high toxicity over the past two decades.Herein,we reported the development of a reduction-responsive drug delive ry system loaded with TP fo r glutathione(GSH)-trigge red drug release for cancer therapy.With the GSH-sensitive TP loaded nanoparticles,the remarkable increases in tumor accumulation and amelioration of drug toxicity in animals are demonstrated,which is likely due to sustained stepwise release of active TP within cancer cells.Moreover,in a patient-derived tumor xenograft model of liver cancer,administration of tritolide nanoparticles enhances the antitumor efficacy relative to administration of free TP.These findings indicate that GSH-sensitive release of TP may be a promising strategy for cancer treatment. 展开更多
关键词 Triptolide Hepatocellular carcinoma Reduction-sensitive polymer Patient-derived xenografts Drug therapy
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Triptolide prolonged allogeneic islet graft survival in chemically induced and spontaneously diabetic mice without impairment of islet function 认领 引用 被引量：11
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作者 Xin, Ming-Jun Cui, Shi-Hua +4 位作者 Liu, Shuang Sun, Hai-Chen Li, Fei Sun, Jia-Bang Luo, Bin 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2010年第3期312-318,共7页
BACKGROUND: Triptolide (TPT) is a diterpenoid triepoxide extracted from the Chinese herb Tripterygium wilfordii Hook. F. It exhibits potent immunosuppressive and anti-inflammatory properties. This study was undertaken... BACKGROUND: Triptolide (TPT) is a diterpenoid triepoxide extracted from the Chinese herb Tripterygium wilfordii Hook. F. It exhibits potent immunosuppressive and anti-inflammatory properties. This study was undertaken to investigate its effects on prolongation of islet allograft survival in rodents. Additionally, we investigated whether TPT would be toxic to islet function in vivo. METHODS: We transplanted BALB/c islets to either chemically induced diabetic C57BL/6 mice or spontaneously diabetic non-obese diabetic (NOD) mice. TPT was injected within 2 weeks or continuously, until rejection, in the two combinations. Then, we evaluated the toxicity of TPT on islet function by daily injection to naive BALB/c or diabetic BALB/c that was cured by syngeneic islet transplantation under the kidney capsule. Mice injected with cyclosporine A (CsA) or vehicle served as controls. Intraperitoneal glucose tolerance tests (IPGTTs) performed at 4 and 8 weeks in the naive BALB/c group, and at 2, 4, 6, and 8 weeks in the syngeneic transplanted group. RESULTS: The medium survival time of islets allograft from TPT treated C57BL/6 and NOD recipients were 28.5 days (range 24-30 days, n=10) and 33.0 days (range 15-47 days, n=6), respectively, and they were significantly different from those of the vehicle treated controls, which were 14.0 days (range 13-16 days, n=6) and 5.0 days (range 4-10 days, n=6), respectively (all P<0.0001). The IPGTT demonstrated that there was no difference between the TPT treated and vehicle treated groups, either in the normal or syngeneic transplanted islet BALB/c mice. However, CsA injection impaired islet function in both normal and syngeneic transplanted mice as early as 4 weeks. CONCLUSION: TPT prolonged islets allograft survival in a chemically induced diabetic or an autoimmune diabetic murine model without impairment of islet function. (Hepatobiliary Pancreat Dis Int 2010; 9: 312-318) 展开更多
关键词 glucose tolerance test immunosuppression islet transplantation non-obese diabetic mice triptolide
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Effects of triptolide on hippocampal microglial cells and astrocytes in the APP/PS1 double transgenic mouse model of Alzheimer's disease 认领 引用 被引量：8
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作者 Jian-ming Li Yan Zhang +5 位作者 Liang Tang Yong-heng Chen Qian Gao Mei-hua Bao Ju Xiang De-liang Lei 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第9期1492-1498,共7页
The principal pathology of Alzheimer＇s disease includes neuronal extracellular deposition of amyloid-beta peptides and formation of senile pl aques, which in turn induce neuroinflammation in the brain. Triptolide, a ... The principal pathology of Alzheimer＇s disease includes neuronal extracellular deposition of amyloid-beta peptides and formation of senile pl aques, which in turn induce neuroinflammation in the brain. Triptolide, a natural extract from the vine-like herb Tripterygium wilfordii Hook F, has potent anti-inflammatory and immunosuppressive efficacy. Therefore, we determined if triptolide can inhibit activation and proliferation of microglial cells and astrocytes in the APP/PS1 double transgenic mouse model of Alzheimer＇s disease. We used 1 or 5 μg/kg/d triptolide to treat APP/PS1 double transgenic mice （aged 4-4.5 months） for 45 days. Unbiased stereology analysis found that triptolide dose-dependent- ly reduced the total number of microglial cells, and transformed microglial cells into the resting state. Further, triptolide （5 μg/kg/d） also reduced the total number of hippocampal astrocytes. Our in vivo test results indicate that triptolide suppresses activation and proliferation of microglial cells and astrocytes in the hippocampus of APP/PS 1 double transgenic mice with Alzheimer＇s disease. 展开更多
关键词 nerve regeneration neurodegenerative disease traditional Chinese medicine Tripterygium wilfordii Hook F triptolide Alzheimer＇sdisease amyloid plaques amyloid-β amyloid precursor protein inflammation microglia astrocytes neural regeneration
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The role of neutrophils in triptolide-induced liver injury 认领 引用 被引量：5
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作者 WANG Xin-Zhi ZHANG Shen-Ye +2 位作者 XU Yao ZHANG Lu-Yong JIANG Zhen-Zhou 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2018年第9期653-664,共12页
Triptolide(TP) induces severe liver injury, but its hepatotoxicity mechanisms are still unclear. Inflammatory responses may be involved in the pathophysiology. Neutrophils are the first-line immune effectors for steri... Triptolide(TP) induces severe liver injury, but its hepatotoxicity mechanisms are still unclear. Inflammatory responses may be involved in the pathophysiology. Neutrophils are the first-line immune effectors for sterile and non-sterile inflammatory responses. Thus, the aim of the present study was to investigate the neutrophilic inflammatory response in TP-induced liver injury in C57 BL/6 mice. Our results showed that neutrophils were recruited and accumulated in the liver, which was parallel to or slightly after the development of liver injury. Neutrophils induced release of myeloperoxidase and up-regulation of CD11 b, which caused cytotoxicity and hepatocyte death. Hepatic expressions of CXL1, TNF-α, IL-6, and MCP1 were increased significantly to regulate neutrophils recruitment and activation. Up-regulation of toll like receptors 4 and 9 also facilitated neutrophils infiltration. Moreover, neutrophils depletion using an anti-Gr1 antibody showed mild protection against TP overdose. These results indicated that neutrophils accumulation might be the secondary response, not the cause of TP-induced liver injury. In conclusion, the inflammatory response including neutrophil infiltration may play a role in TP-induced hepatotoxicity, but may not be severe enough to cause additional liver injury. 展开更多
关键词 Triptolide Liver injury Inflammatory response Neutrophil Depletion
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Atractylodes lancea rhizome water extract reduces triptolide-induced toxicity and enhances anti-inflammatory effects 认领 引用 被引量：5
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作者 WEI Yuan SUI Dan-Juan +5 位作者 XU Hai-Miao OUYANG Zhen WU Na WANG Du-Jun ZHANG Xiao-Yan QIAN Da-Wei 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2017年第12期905-911,共7页
The present study was designed to explore the influence of water extracts of Atractylodes lancea rhizomes on the toxicity and anti-inflammatory effects of triptolide(TP). A water extract was prepared from A. lancea rh... The present study was designed to explore the influence of water extracts of Atractylodes lancea rhizomes on the toxicity and anti-inflammatory effects of triptolide(TP). A water extract was prepared from A. lancea rhizomes and co-administered with TP in C57BL/6 mice. The toxicity was assayed by determining serum biochemical parameters and visceral indexes and by liver histopathological analysis. The hepatic CYP3A expression levels were detected using Western blotting and RT-PCR methods. The data showed that the water extract of A. lancea rhizomes reduced triptolide-induced toxicity, probably by inducing the hepatic expression of CYP3A. The anti-inflammatory effects of TP were evaluated in mice using a xylene-induced ear edema test. By comparing ear edema inhibition rates, we found that the water extract could also increase the anti-inflammatory effects of TP. In conclusion, our results suggested that the water extract of A. lancea rhizomes, used in combination with TP, has a potential in reducing TP-induced toxicity and enhancing its anti-inflammatory effects. 展开更多
关键词 Triptolide Atractylodes lancea Licorice CYP3A Anti-inflammation effects
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Inhibitive effect of triptolide on invasiveness of human fibrosarcoma cells by downregulating matrix metalloproteinase-9 expression 认领 引用 被引量：4
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作者 Shengbo Yang Can Gu +4 位作者 Guiying Zhang Jian Kang Haiquan Wen QianJin Lu Jinhua Huang 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2011年第6期482-485,共4页
Objective:To explore the molecular mechanisms of antitumor properties of triptolide,a bioactive component isolated from the Chinese herb Tripterygium wolfordii Hook F.Methods:Human fibrosarcoma HT-1080 cells were trea... Objective:To explore the molecular mechanisms of antitumor properties of triptolide,a bioactive component isolated from the Chinese herb Tripterygium wolfordii Hook F.Methods:Human fibrosarcoma HT-1080 cells were treated with different doses of triptolide for 72 h.Then the expression and activity of matrix metalloproteinase(MMP)-2 and -9 were measured and the invasiveness of triptolide-treated HT-1080 cells was compared with that of anti-MMP-9- treated HT-1080 cells.Results:18 nmol/L triptolide inhibited the gene expression and activity of MMP-9,but not those of MMP-2,in HT-1080 cells.In addition,both 18 nmol/L triptolide and 3μg/mL anti-MMP-9 significantly reduced the invasive potential of HT-1080 cells,by about 50%and 35%, respectively,compared with the control.Whereas there was no significant difference between the effect of 18 nmol/L triptolide and that of anti-MMP-9 on invasive potential of HT-1080 cells. Conclusions:These data suggest that triptolide inhibits tumor cell invasion partly by reducing MMP-9 gene expression and activity. 展开更多
关键词 Triptolide Matrix metalloproteinase Fibrosarcoma Neoplasm metastasis
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Differential expression of the TwHMGS gene and its effect on triptolide biosynthesis in Tripterygium wilfordii 认领 引用 被引量：4
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作者 TONG Yu-Ru ZHANG Yi-Feng +4 位作者 ZHAO Yu-Jun HU Tian-Yuan WANG Jia-Dian HUANG Lu-Qi GAO Wei 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2019年第8期575-584,共10页
3-Hydroxy-3-methylglutaryl-CoA synthase(HMGS) is the first committed enzyme in the MVA pathway and involved in the biosynthesis of terpenes in Tripterygium wilfordii. The full-length cDNA and a 515 bp RNAi target frag... 3-Hydroxy-3-methylglutaryl-CoA synthase(HMGS) is the first committed enzyme in the MVA pathway and involved in the biosynthesis of terpenes in Tripterygium wilfordii. The full-length cDNA and a 515 bp RNAi target fragment of TwHMGS were ligated into the p H7 WG2 D and p K7 GWIWG2 D vectors to respectively overexpress and silence, Tw HMGS was overexpressed and silenced in T. wilfordii suspension cells using biolistic-gun mediated transformation, which resulted in 2-fold increase and a drop to70% in the expression level compared to cells with empty vector controls. During Tw HMGS overexpression, the expression of TwHMGR, TwDXR and TwTPS7 v2 was significantly upregulated to the control. In the RNAi group, the expression of Tw HMGR,TwDXS, TwDXR and TwMCT visibly displayed downregulation to the control. The cells with TwHMGS overexpressed produced twice higher than the control value. These results proved that differential expression of Tw HMGS determined the production of triptolide in T.wilfordii and laterally caused different trends of relative gene expression in the terpene biosynthetic pathway. Finally, the substrate acetyl-Co A was docked into the active site of TwHMGS, suggesting the key residues including His247, Lys256 and Arg296 undergo electrostatic or H-bond interactions with acetyl-CoA. 展开更多
关键词 Overexpression RNAi HMGS Triptolide Acetyl-CoA
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A single-cell landscape of triptolide-associated testicular toxicity in mice 认领 引用 被引量：4
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作者 Wei Zhang Siyu Xia +5 位作者 Jinhuan Ou Min Cao Guangqing Cheng Zhijie Li Jigang Wang Chuanbin Yang 《Journal of Pharmaceutical Analysis》 SCIE CAS CSCD 2023年第8期880-893,共14页
Triptolide is a key active component of the widely used traditional Chinese herb medicine Tripterygium wilfordii Hook.F.Although triptolide exerts multiple biological activities and shows promising efficacy in treatin... Triptolide is a key active component of the widely used traditional Chinese herb medicine Tripterygium wilfordii Hook.F.Although triptolide exerts multiple biological activities and shows promising efficacy in treating inflammatory-related diseases,its well-known safety issues,especially reproductive toxicity has aroused concerns.However,a comprehensive dissection of triptolide-associated testicular toxicity at single cell resolution is still lacking.Here,we observed testicular toxicity after 14 days of triptolide exposure,and then constructed a single-cell transcriptome map of 59,127 cells in mouse testes upon triptolide-treatment.We identified triptolide-associated shared and cell-type specific differentially expressed genes,enriched pathways,and ligand-receptor pairs in different cell types of mouse testes.In addition to the loss of germ cells,our results revealed increased macrophages and the inflammatory response in triptolide-treated mouse testes,suggesting a critical role of inflammation in triptolide-induced testicular injury.We also found increased reactive oxygen species(ROS)signaling and downregulated pathways associated with spermatid development in somatic cells,especially Leydig and Sertoli cells,in triptolide-treated mice,indicating that dysregulation of these signaling pathways may contribute to triptolide-induced testicular toxicity.Overall,our high-resolution single-cell landscape offers comprehensive information regarding triptolide-associated gene expression profiles in major cell types of mouse testes at single cell resolution,providing an invaluable resource for understanding the underlying mechanism of triptolide-associated testicular injury and additional discoveries of therapeutic targets of triptolide-induced male reproductive toxicity. 展开更多
关键词 Single-cell sequence Transcriptomics Triptolide Reproduction toxicity Testis
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