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Obakulactone Alleviates Rheumatoid Arthritis by Promotion of ACOT1 Degradation via the Ubiquitin‒Proteasome Pathway and Restoration of Unsaturated Fatty Acid Homeostasis 认领 引用
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作者 Hongda Liu Le Yang +12 位作者 Yu Yang Huan Tang Junling Ren Hui Sun Xin Sun Songyuan Tang Chong Qiu Ye Sun Jigang Wang Guangli Yan Ling Kong Ying Han Xijun Wang 《Engineering》 SCIE EI CSCD 2026年第1期341-360,共20页
Rheumatoid arthritis(RA)remains a therapeutic challenge because of the suboptimal efficacy and significant adverse effects of current treatments.Obakulactone(OL),a natural tetracyclic triterpenoid isolated from Phello... Rheumatoid arthritis(RA)remains a therapeutic challenge because of the suboptimal efficacy and significant adverse effects of current treatments.Obakulactone(OL),a natural tetracyclic triterpenoid isolated from Phellodendri cortex,has emerged as a promising candidate for RA intervention.However,its underlying mechanism remains poorly understood.In this study,we investigated the therapeutic effects of OL and its molecular mechanisms in RA using a multifaceted approach.A complete Freund's adjuvant(CFA)-induced RA rat model revealed that OL significantly alleviated joint swelling and restored the expression of CD3+T cells and CD68+macrophages in joints,and the polarization state of macrophages shifted from proinflammatory M1(CD86)to anti-inflammatory M2(CD206)dominant.In addition,OL alleviated pathological changes in lymphoid organs(thymus and spleen),effectively inhibited the differentiation of CD4+T cells into T helper 17(Th17)cells,and normalized serum levels of inflammatory cytokines(e.g.,interleukin(IL)-6 and tumor necrosis factor-α(TNF-α))and RA diagnostic markers(e.g.,creactive protein(CRP)and rheumatoid factor(RF)).Multiomics profiling revealed that OL corrected the dysregulated biosynthesis and metabolism of unsaturated fatty acids(e.g.,arachidonic acid and linolenic acid)in RA rats,with acyl coenzyme A(CoA)thioesterase 1(ACOT1)identified as a critical regulator.In vitro studies have shown that OL significantly inhibits cell proliferation and inflammatory cytokine secretion and promotes the apoptosis of RA synovial fibroblasts(SFs).It inhibited the M1 polarization of Raw264.7 macrophages and promoted M2 polarization.Mechanistically,cellular thermal shift assays(CETSA),microscale thermo phoresis(MST),surface plasmon resonance(SPR),and short hairpin RNA(shRNA)experiments revealed ACOT1 as the direct target of OL.OL enhanced ACOT1 ubiquitinationmediated proteasomal degradation,thereby reducing downstream stearoyl-CoA desaturase-1 expression and inhibiting the Janus kinase(JAK)-signal transducer and activator of transcription(STAT)and phosphoinositide 3-kinase(PI3K)-protein kinase B(AKT)signaling pathways,thus suppressing inflammation and fibrosis in SFs.This study establishes OL as a potential RA therapeutic agent and highlights ACOT1 as a novel target for RA intervention,offering insights into fatty acid metabolism reprogramming as a therapeutic strategy. 展开更多
关键词 Obakulactone Rheumatoid arthritis Unsaturated fatty acids Acyl coenzyme A thioesterase 1 Synovial fibroblasts Multiomics Ubiquitin-proteasome pathway
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Oridonin mitigates cerebral ischemic-reperfusion injury via covalent binding to HMGB1 and inhibiting the HMGB1/TLR4/MyD88/NF-κB signaling pathway 认领 引用
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作者 Dandan Liu Shujie Zhang +13 位作者 Fei Xia Qiaoli Shi Hui Zhao Yinkwan Wong Yuqing Meng Yanqing Liu Yongping Zhu Xin Chai Jiale Xing Huan Tang Chong Qiu Peili Wang Ang Ma Jigang Wang 《Acupuncture and Herbal Medicine》 CAS CSCD 2026年第1期56-72,共17页
Objective:Ischemic stroke(IS)is a leading cause of mortality and disability worldwide,and effective pharmacological treatments are limited.Oridonin(Ori)has demonstrated neuroprotective potential in IS;however,its unde... Objective:Ischemic stroke(IS)is a leading cause of mortality and disability worldwide,and effective pharmacological treatments are limited.Oridonin(Ori)has demonstrated neuroprotective potential in IS;however,its underlying mechanisms are still poorly understood.Methods:In vitro,oxygen-glucose deprivationeperfusion(OGD/R)models were established using mouse neuroblastoma Neuro-2a cells and primary cortical neurons.In vivo,a transient middle cerebral artery occlusion(tMCAO)model was induced in male C57BL/6J mice to simulate cerebral ischemic–reperfusion(I/R)injury.The key targets of Ori were identified using activitybased protein profiling(ABPP).The binding affinity between Ori and its target protein was validated using multiple approaches,including cellular thermal shift assay(CETSA),molecular docking,and biolayer interferometry(BLI).Results:Ori significantly suppressed the expression of inflammatory cytokines in tMCAO-and OGD/R-treated neuronal cells.Target identification revealed that high-mobility group box 1(HMGB1)protein is the key mediator of the protective effects of Ori against cerebral I/R injury.Mechanistically,Ori covalently binds to cysteine(Cys)106 of HMGB1,reducing its secretion and proinflammatory activity.Additionally,Ori downregulated cytoplasmic HMGB1 levels and the expression of TLR4 and MyD88,as well as the p-p65/p65 ratio in both OGD/R and tMCAO models.Notably,the HMGB1 inhibitor NecroX-7 conferred protection against OGD/R-induced neuronal injury and tMCAO-induced brain damage in mice,which could not be further modulated by Ori treatment.Conclusions:Our findings demonstrate that Ori confers neuroprotection against brain I/R injury by covalently binding to HMGB1 at Cys106 via its reactive carbon–carbon double bonds,thereby eliminating the proinflammatory activity of HMGB1.This molecular interaction reduces HMGB1 secretion and inhibits the downstream HMGB1/TLR4/MyD88/NF-κB signaling pathway,ultimately attenuating neuroinflammation and ischemic damage. 展开更多
关键词 Cerebral ischemic-reperfusion injury Chemical proteomics HMGB1 Oridonin Target discovery
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Single-cell transcriptome analysis uncovers underlying mechanisms of acute liver injury induced by tripterygium glycosides tablet in mice 认领 引用 被引量：6
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作者 Qiuyan Guo Jiangpeng Wu +14 位作者 Qixin Wang Yuwen Huang Lin Chen Jie Gong Maobo Du Guangqing Cheng Tianming Lu Minghong Zhao Yuan Zhao Chong Qiu Fei Xia Junzhe Zhang Jiayun Chen Feng Qiu Jigang Wang 《Journal of Pharmaceutical Analysis》 SCIE CAS CSCD 2023年第8期908-925,共18页
Tripterygium glycosides tablet(TGT),the classical commercial drug of Tripterygium wilfordii Hook.F.has been effectively used in the treatment of rheumatoid arthritis,nephrotic syndrome,leprosy,Behcet's syndrome,le... Tripterygium glycosides tablet(TGT),the classical commercial drug of Tripterygium wilfordii Hook.F.has been effectively used in the treatment of rheumatoid arthritis,nephrotic syndrome,leprosy,Behcet's syndrome,leprosy reaction and autoimmune hepatitis.However,due to its narrow and limited treatment window,TGT-induced organ toxicity(among which liver injury accounts for about 40%of clinical reports)has gained increasing attention.The present study aimed to clarify the cellular and molecular events underlying TGT-induced acute liver injury using single-cell RNA sequencing(scRNA-seq)technology.The TGT-induced acute liver injury mouse model was constructed through short-term TGT exposure and further verified by hematoxylin-eosin staining and liver function-related serum indicators,including alanine aminotransferase,aspartate aminotransferase,alkaline phosphatase and total bilirubin.Using the mouse model,we identified 15 specific subtypes of cells in the liver tissue,including endothelial cells,hepatocytes,cholangiocytes,and hepatic stellate cells.Further analysis indicated that TGT caused a significant inflammatory response in liver endothelial cells at different spatial locations;led to marked inflammatory response,apoptosis and fatty acid metabolism dysfunction in hepatocytes;activated hepatic stellate cells;brought about the activation,inflammation,and phagocytosis of liver capsular macrophages cells;resulted in immune dysfunction of liver lymphocytes;disturbed the intercellular crosstalk in liver microenvironment by regulating various signaling pathways.Thus,these findings elaborate the mechanism underlying TGT-induced acute liver injury,provide new insights into the safe and rational applications in the clinic,and complement the identification of new biomarkers and therapeutic targets for liver protection. 展开更多
关键词 Tripterygium glycosides tablet Acute liver injury scRNA-seq
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In vitro comparative evaluation of three CLD/siRNA nanoplexes prepared by different processes 认领 引用 被引量：2
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作者 Chong Qiu Shihe Cui +1 位作者 Jing Sun Jiancheng Wang 《Journal of Chinese Pharmaceutical Sciences》 CAS CSCD 2016年第9期660-668,共9页
In this study, a gemini-like cationic lipid （CLD） was used as the carrier to study the complexation features of CLD/ siRNA nanoplexes （CLD/siRNA NPs）. Three types of CLD/siRNA nanoplexes （named as AT NPs, HT NPs ... In this study, a gemini-like cationic lipid （CLD） was used as the carrier to study the complexation features of CLD/ siRNA nanoplexes （CLD/siRNA NPs）. Three types of CLD/siRNA nanoplexes （named as AT NPs, HT NPs and MT NPs） were prepared by different processes： AT method （mixing siRNA solution with preformed CLD nanoparticles）, HT method （hydrating a CLD thin film with siRNA solution）, and MT method （dropping an ethanolic solution of CLD into siRNA solution under sonication）. The particle size, zeta potential, morphology, siRNA protection, cytotoxicity, cellular uptake, and targeted mRNA downregulation were studied. At the optimal N/P ratio of 10, the sizes of the three CLD/siRNA NPs were MT NPs （（222.3±19.1） nm）〉 HT NPs （（105.7±1.31） nm）〉AT NPs （（91.8±1.75） nm）. Different nanostructures were formed despite the fact that they were composed of the same components. Furthermore, the TEM images indicated that different morphologies were found in the three NPs, indicating that the nanoplexes were assembled by different mechanisms. Among the three NPs, the cell uptake capacity were as follows： AT NPs〉MT NPs〉HT NPs, whereas the silencing levels on epidermal growth factor receptor （EGFR） in HeLa cells were MT NPs〉AT NPs〉HT NPs. Based on the above results, we hypothesized that the different preparation processes resulted in nanostructures with varying biological effects. Therefore, we believe that structural optimization of siRNA nanoplexes is essential in achieving better siRNA encapsulation, protection, and gene silencing efficiency. 展开更多
关键词 siRNA Delivery Nanoparticles Preparation Cellular uptake
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A highly efficient protein corona-based proteomic analysis strategy for the discovery of pharmacodynamic biomarkers 认领 引用
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作者 Yuqing Meng Jiayun Chen +15 位作者 Yanqing Liu Yongping Zhu Yin-Kwan Wong Haining Lyu Qiaoli Shi Fei Xia Liwei Gu Xinwei Zhang Peng Gao Huan Tang Qiuyan Guo Chong Qiu Chengchao Xu Xiao He Junzhe Zhang Jigang Wang 《Journal of Pharmaceutical Analysis》 SCIE CAS CSCD 2022年第6期879-888,共10页
The composition of serum is extremely complex,which complicates the discovery of new pharmacodynamic biomarkers via serum proteome for disease prediction and diagnosis.Recently,nanoparticles have been reported to effi... The composition of serum is extremely complex,which complicates the discovery of new pharmacodynamic biomarkers via serum proteome for disease prediction and diagnosis.Recently,nanoparticles have been reported to efficiently reduce the proportion of high-abundance proteins and enrich lowabundance proteins in serum.Here,we synthesized a silica-coated iron oxide nanoparticle and developed a highly efficient and reproducible protein corona(PC)-based proteomic analysis strategy to improve the range of serum proteomic analysis.We identified 1,070 proteins with a median coefficient of variation of 12.56%using PC-based proteomic analysis,which was twice the number of proteins identified by direct digestion.There were also more biological processes enriched with these proteins.We applied this strategy to identify more pharmacodynamic biomarkers on collagen-induced arthritis(CIA)rat model treated with methotrexate(MTX).The bioinformatic results indicated that 485 differentially expressed proteins(DEPs)were found in CIA rats,of which 323 DEPs recovered to near normal levels after treatment with MTX.This strategy can not only help enhance our understanding of the mechanisms of disease and drug action through serum proteomics studies,but also provide more pharmacodynamic biomarkers for disease prediction,diagnosis,and treatment. 展开更多
关键词 Protein corona Nanoparticles Mass spectrometry Proteomic analysis Pharmacodynamic biomarkers
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Gambogenic acid ameliorates inflammation by inhibiting HK1-mediated Warburg effect and NLRP3 inflammasome activation in sepsis 认领 引用 被引量：1
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作者 Huanhuan Pang Honglin Chen +18 位作者 Peng Chen Xu Wei Hongda Liu Xueling He Yang Yang Junzhe Zhang Dianfei Li Linlin Lou Wen Xie Chong Qiu Fei Xia Qiuyan Guo Shengnan Shen Qiaoli Shi Weiguang Li Guang Han Xijun Wang Jigang Wang Chengchao Xu 《Acta Pharmaceutica Sinica B》 SCIE CAS CSCD 2026年第1期337-351,共15页
Sepsis is a life-threatening disease caused by the dysregulated host immune response to infection, which eventually leads to multi-organ failure. Current therapeutic strategies rely heavily on antibiotics. However, co... Sepsis is a life-threatening disease caused by the dysregulated host immune response to infection, which eventually leads to multi-organ failure. Current therapeutic strategies rely heavily on antibiotics. However, conventional antimicrobial therapy often leads to antibiotic abuse and resistance. Therefore, it is of utmost importance to develop new agents for treating sepsis. Here, we demonstrated that gambogenic acid (GNA) not only restricted the release of inflammatory cytokines in lipopolysaccharide (LPS)-stimulated macrophages but also attenuated the inflammatory response and organ damage in septic mice. By using the activity-based protein profiling (ABPP) strategy, we identified 30 potential target proteins of GNA. Among these potential targets, we found that GNA directly bound to the Cys684 residue of hexokinase 1 (HK1) and affected its enzyme activity and cellular localization. These findings were confirmed by the cellular thermal shift assay (CETSA), bio-layer interferometry (BLI), and single-site mutation experiments. Functionally, siHK1 alleviated the Warburg effect, suppressed the activation of NLRP3 inflammasome, and eventually suppressed the release of inflammatory cytokines. Taken together, our findings demonstrated that GNA could attenuate inflammation by alleviating HK1-mediated Warburg effect and NLRP3 inflammasome activation in sepsis and could serve as a novel therapeutic agent for sepsis and inflammatory disorders. 展开更多
关键词 Inflammation Activity-based protein profiling(ABPP) Target identification Chemical proteomics Gambogenic acid(GNA) Hexokinase 1(HK1) Warburg effect Sepsis
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Rhein/Fe3+nanoassembly for triple-negative breast cancer treatment via a ferroptosis and immunogenic death 认领 引用
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作者 Shuntao Liang Licheng Gan +10 位作者 Xiaomei Tao Fei Xia Qingchao Tu Linying Zhong Yuanfeng Fu Yinan Liu Yuqing Meng Qiaoli Shi Junzhe Zhang Jigang Wang Chong Qiu 《Chinese Herbal Medicines》 CAS CSCD 2026年第2期481-483,共3页
To the Editor:Triple-negative breast cancer(TNBC)remains one of the most formidable clinical challenges in oncology.Due to the absence of estrogen receptor,progesterone receptor,and human epidermal growth factor recep... To the Editor:Triple-negative breast cancer(TNBC)remains one of the most formidable clinical challenges in oncology.Due to the absence of estrogen receptor,progesterone receptor,and human epidermal growth factor receptor(HER2)expression,TNBC is intrinsically insensitive to endocrine therapies and HER2-targeted agents.Although immune checkpoint blockade(ICB)has transformed cancer therapy,its efficacy in TNBC is often limited by an“immune-cold”microenvironment characterized by scarce tumor-infiltrating lymphocytes and dominant immunosuppressive(Keenan&Tolaney,2020). 展开更多
关键词 Rhein triple negative breast cancer ferroptosis endocrine therapies human epidermal growth factor Fe immunogenic death immune checkpoint blockade icb
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Dihydroartemisinin Regulated the MMP-Mediated Cellular Microenvironment to Alleviate Rheumatoid Arthritis 认领 引用 被引量：8
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作者 Qiuyan Guo Qixin Wang +15 位作者 Jiayun Chen Minghong Zhao Tianming Lu Zuchang Guo Chen Wang Yin Kwan Wong Xueling He Lin Chen Wenjing Zhang Chuanhao Dai Shengnan Shen Huanhuan Pang Fei Xia Chong Qiu Daoyuan Xie Jigang Wang 《Research》 SCIE EI CSCD 2025年第2期627-640,共14页
Rheumatoid arthritis(RA)is an autoimmune disease with features of synovial inflammation,cartilage erosion,bone destruction,and pain and is currently lacking a satisfactory treatment strategy.Dihydroartemisinin(DHA),th... Rheumatoid arthritis(RA)is an autoimmune disease with features of synovial inflammation,cartilage erosion,bone destruction,and pain and is currently lacking a satisfactory treatment strategy.Dihydroartemisinin(DHA),the active metabolite of artemisinin,has exhibited outstanding suppressive effects on RA without obvious side effects.However,the underlying mechanisms remain unclear,which limits its further clinical application.The purpose of this study is to reveal the pharmacodynamic mechanism of DHA against RA by means of a combination of single-cell RNA sequencing(RNA-seq),proteomics,as well as transcriptomics both invivo and invitro.In our results,DHA effectively reduced the degree of redness,swelling,and pain in RA rats and dramatically changed the synovial tissue microenvironment under the pathological state.Within this microenvironment,fibroblasts,macrophages,B cells,and endothelial cells were the major affected cell types,primarily through DHA targeting the extracellular matrix(ECM)structural constituent signaling pathway.In addition,we confirmed that DHA regulated the ECM by modulating matrix metalloproteinase 2(MMP2)and MMP3 in the synovial tissue of RA rats.Moreover,DHA induced apoptosis in MH7A cells,further validating the bioinformatics data.In conclusion,DHA effectively reduced the inflammatory response and improved the immune microenvironment in synovial tissue by inhibiting MMP2 and MMP3.Our findings provide a basis for the application of DHA in the treatment of RA. 展开更多
关键词 reveal pharmacodynamic mechanism proteomics rheumatoid arthritis ra active metabolite dihydroartemisinin single cell RNA sequencing synovial inflammationcartilage rheumatoid arthritis
RDYH58 functional exosomes targeting myofibroblasts loaded with siFKBP10 for inhibition of collagen biosynthesis and secretion of IPF 认领 引用 被引量：2
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作者 Ranran Yuan Zhen Mu +12 位作者 Houqian Zhang Yu Tian Quanlin Xin Qingchao Tu Yan Zhang Yanqiu Li Zhiwen Zhang Yongchao Chu Aiping Wang Jingwei Tian Hongbo Wang Chong Qiu Yanan Shi 《Acta Pharmaceutica Sinica B》 SCIE CAS CSCD 2025年第12期6681-6697,共17页
Idiopathic pulmonary fibrosis(IPF)is a complex interstitial lung disease in which myofibroblasts are the primary effector cells.FK506-binding protein(FKBP10),a procollagen chaperone,is upregulated in IPF and primarily... Idiopathic pulmonary fibrosis(IPF)is a complex interstitial lung disease in which myofibroblasts are the primary effector cells.FK506-binding protein(FKBP10),a procollagen chaperone,is upregulated in IPF and primarily localizes to myofibroblasts.Exosomes have garnered significant attention as novel drug delivery vehicles,particularly when engineered.However,myofibroblasts remain underexplored in terms of engineered exosome-based therapies and associated drug targets.In this study,RDYH58,a peptide that targets myofibroblasts,was conjugated to the exosomal membrane protein Lamp2b to produce RDYH58-linked exosomes(RDYH58-exo).In vitro and in vivo experiments demonstrated that compared to unmodified exosomes(unm-exo),RDYH58-exo preferentially localized to myofibroblasts.A small interfering RNA targeting FKBP10(siFKBP10)was loaded into exosomes using ultrasonic microfluidics method,and the antifibrotic effects of RDYH58-exo carrying siFKBP10(RDYH58-siFKBP10)were assessed both in vitro and in vivo.The results demonstrated that RDYH58-siFKBP10 effectively silenced FKBP10 gene expression,significantly inhibiting fibroblast activation and extracellular matrix deposition,with superior antifibrotic efficacy compared to unmodified exosome vectors(unm-siFKBP10).RNA-seq analysis confirmed the pivotal regulatory role of FKBP10,providing critical evidence for the development of targeted therapeutic strategies.The RDYH58-siFKBP10 delivery system developed in this study demonstrates remarkable clinical translation potential. 展开更多
关键词 Idiopathic pulmonary fibrosis Myofibroblasts FK506-Binding protein RDYH58 Exosomes Drug delivery Small interfering RNA Ultrasonic microfluidics method
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Review of HVDC Tap 认领 引用
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作者 Chong Qiu Songtao Huang Yihua Hu 《Chinese Journal of Electrical Engineering》 EI CSCD 2025年第1期1-15,共15页
The development of high-voltage direct current(HVDC)systems has been pivotal to the evolution of modern power systems,particularly in terms of providing an effective solution for long-distance,high-capacity power tran... The development of high-voltage direct current(HVDC)systems has been pivotal to the evolution of modern power systems,particularly in terms of providing an effective solution for long-distance,high-capacity power transmission,which has become increasingly important in the integration of renewable energy technologies.The integration of renewable energy sources into the grid requiresthe use of sophisticated tap-changing technology to ensure efficient extraction of power from HVDC lines.A critical review of the current status of the HVDC technologyis presentedin this paper.It synthesizes research findings on power flow optimization,grid expansion,and the challenges of designing HVDC grid substations.The development of modular multilevel converters(MMCs)and DC-DC converters,particularly for use in hybrid alternating current(AC)/direct current(DC)grids,is highlighted.These findings emphasize the importance of continuous research on the HVD Ctap technology to improve the efficiency,reliability,and scalability of future power systems. 展开更多
关键词 High-voltage direct current(HVDC) modular multilevel converter(MMC) tapping topologies power systems
Advanced Strategies for Overcoming Endosomal/Lysosomal Barrier in Nanodrug Delivery 认领 引用 被引量：1
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作者 Chong Qiu Fei Xia +8 位作者 Junzhe Zhang Qiaoli Shi Yuqing Meng Chen Wang Huanhuan Pang Liwei Gu Chengchao Xu Qiuyan Guo Jigang Wang 《Research》 SCIE EI CSCD 2024年第1期315-337,共23页
Nanocarriers have therapeutic potential to facilitate drug delivery,including biological agents,smallmolecule drugs,and nucleic acids.However,their efficiency is limited by several factors;among which,endosomal/lysoso... Nanocarriers have therapeutic potential to facilitate drug delivery,including biological agents,smallmolecule drugs,and nucleic acids.However,their efficiency is limited by several factors;among which,endosomal/lysosomal degradation after endocytosis is the most important.This review summarizes advanced strategies for overcoming endosomal/lysosomal barriers to efficient nanodrug delivery based on the perspective of cellular uptake and intracellular transport mechanisms.These strategies include promoting endosomal/lysosomal escape,using non-endocytic methods of delivery to directly cross the cell membrane to evade endosomes/lysosomes and making a detour pathway to evade endosomes/lysosomes.On the basis of the findings of this review,we proposed several promising strategies for overcoming endosomal/lysosomal barriers through the smarter and more efficient design of nanodrug delivery systems for future clinical applications. 展开更多
关键词 somal drugs finding
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