机构地区:[1]School of Traditional Chinese Medicine,Beijing University of Chinese Medicine,Beijing 102488,China [2]Modern Research Center for Traditional Chinese Medicine,Beijing University of Chinese Medicine,Beijing 102488,China [3]Department of Cellular&Molecular Physiology,Institute of Translational Medicine,University of Liverpool,Liverpool,L693BX,United Kingdom [4]Shenzhen Institutes of Advanced Technology,Chinese Academy of Sciences,Shenzhen 518055,China [5]State Key Laboratory of Traditional Chinese Medicine Syndrome,Guangzhou University of Chinese Medicine,Guangzhou 510006,China [6]Key Laboratory of TCM Syndrome and Formula,Beijing University of Chinese Medicine,Ministry of Education,Beijing 102488,China [7]Department of Geriatrics,Zhengzhou Hospital of Traditional Chinese Medicine,Zhengzhou 450007,China [8]Institute of Geriatric Diseases,Henan Academy of Traditional Chinese Medicine,Zhengzhou 450046,China
出 处:《Journal of Traditional Chinese Medical Sciences》2025年第1期31-43,共13页中医科学杂志(英文)
基 金:supported the National Natural Science Foundation of China(81930113).
摘 要:Objective:To investigate the potential protective effect of Shexiang Tongxin dropping pills(STDP)on ischemia-reperfusion injury and its underlying mechanisms in improving endothelial cell function in coronary microvascular disease(CMVD).Methods:A rat model of myocardial ischemia-reperfusion injury with CMVD was established using ligation and reperfusion of the left anterior descending artery.The effect of STDP(21.6 mg/kg)on cardiac function was evaluated using echocardiography,hematoxylin-eosin staining,and Evans blue staining.The effects of STDP on the microvascular endothelial barrier were assessed based on nitric oxide production,endothelial nitric oxide synthase expression,structural variety of tight junctions(TJs),and the expression of zonula occludens-1(ZO-1),claudin-5,occludin,and vascular endothelial(VE)-cadherin proteins.The mechanisms of STDP(50 and 100 ng/mL)were evaluated by examining the expression of sphingosine 1-phosphate receptor 2(S1PR2),Ras Homolog family member A(RhoA),and Rho-associated coiled-coil-containing protein kinase(ROCK)proteins and the distribution of ZO-1,VE-cadherin,and Factin proteins in an oxygen and glucose deprivation/reoxygenation model.Results:The administration of STDP on CMVD rat model significantly improved cardiac and microvascular endothelial cell barrier functions(all P<.05).STDP enhanced the structural integrity of coronary microvascular positioning and distribution by clarifying and completing TJs and increasing the expression of ZO-1,occludin,claudin-5,and VE-cadherin in vivo(all P<.05).The S1PR2/RhoA/ROCK pathway was inhibited by STDP in vitro,leading to the regulation of endothelial cell TJs,adhesion junctions,and cytoskeletal morphology.Conclusion:STDP showed protective effects on cardiac impairment and microvascular endothelial barrier injury in CMVD model rats induced by myocardial ischemia-reperfusion injury through the modulation of the S1PR2/RhoA/ROCK pathway.
关 键 词:Coronary artery microvascular disease Shexiang Tongxin dropping pills Ischemia-reperfusion injury Microvascular barrier function S1PR2/RhoA/ROCK pathway
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