Background Skeletal muscle has recently been recognized as an endocrine organ that can express, synthesize and secrete a variety of bioactive molecules which exert significant regulatory effects. Hydrogen sulfide （H2...Background Skeletal muscle has recently been recognized as an endocrine organ that can express, synthesize and secrete a variety of bioactive molecules which exert significant regulatory effects. Hydrogen sulfide （H2S） iS endogenously produced in mammalian tissues and participates in a number of physiological and pathophysiological processes. We aimed to verify whether H2S could be endogenously generated and released by rat skeletal muscle, and determine the biological effects of H2S in rat skeletal muscle. Methods The study was divided into two parts： detection of endogenous H2S generation and release in rat skeletal muscle and determination of antioxidative activity of skeletal muscle-derived H2S. H2S content and production in tissues were ,detected by sensitive sulfur electrode method. The expressions of H2S producing enzymes cystathionine i^-synthase, cystathionine y-lyase and mercaptopyruvate sulfurtransferase were detected by real-time PCR and western blotting and their tissue distributions were observed by immunohistochemical and immunofluorescent analysis. Rat skeletal muscular ischemia-reperfusion （I-R） injury model was created and evaluated by histological analysis under microscope. The malondialdehyde （MDA） contents, hydrogen peroxide levels, superoxide anion and superoxide dismutase （SOD） activities were detected using spectrophotometer. Results H2S could be endogenously generated and released by skeletal muscle of Sprague-Dawley rats （H2S content： （2.06＋0.43） nmol/mg; H2S production： （0.17＋0.06） nmol.minl.mgl）. Gene and protein expressions of the three H2S producing enzymes ~vere detected in skeletal muscle, as well as the liver and kidney. Endogenous H2S content and production were decreased in skeletal muscles of rats with I-R skeletal muscle injury （P 〈0.05）. Furthermore, H2S significantly protected rat skeletal muscle against I-R injury and resulted in decreased MDA content, reduced hydrogen peroxide and superoxide anion levels, but increased SOD activi展开更多
目的研究缺血后适应对急性ST段抬高型心肌梗死(STEMI)患者心脏结构及功能的影响。方法全面检索Medline、Embase、the Cochrane Central Register of Controlled Trials、中国生物医学文献数据库、中国知网、万方数据库及维普期刊数据库...目的研究缺血后适应对急性ST段抬高型心肌梗死(STEMI)患者心脏结构及功能的影响。方法全面检索Medline、Embase、the Cochrane Central Register of Controlled Trials、中国生物医学文献数据库、中国知网、万方数据库及维普期刊数据库,检索时间为从建库至2018年4月30日。主要结局指标为最终梗死面积、左心室射血分数,次要结局指标为心肌水肿程度、心肌挽救指数、微循环障碍发生率、左心室舒张末期容积。以上所有指标均通过心脏核磁共振成像评估及量化。结果共有12个研究纳入Meta分析。对于STEMI患者,冠状动脉内缺血后适应联合经皮冠状动脉介入治疗(PCI)与单纯PCI相比,可以显著减少最终心肌梗死面积(SMD–0.19,95%CI–0.38～0.00,P=0.048),可以显著增加左心室射血分数(WMD 1.62,95%CI0.39～2.85,P=0.010)及心肌挽救指数(WMD 3.69,95%CI0.25～7.13,P=0.035),有降低心肌水肿的趋势(SMD–0.18,95%CI–0.38～0.01,P=0.057),但未能显著降低微循环障碍发生率(RR 0.98,95%CI 0.84～1.14,P>0.05),未能减小左心室舒张末期容积(WMD–0.15,95%CI–3.05～2.74,P>0.05)。结论对于STEMI患者,缺血后适应联合PCI可以降低最终梗死面积、增加左心室射血分数及心肌挽救指数,并有降低心肌水肿的趋势,对心脏有显著保护作用,但未能降低微循环障碍发生率及左心室舒张末期容积。展开更多
基金The study was supported by the grants from Major Basic Research Development Program of People＇s Republic of China （No. 2011CB503904 and No. 2013CB933801） and National Natural Science Foundation of China （No. 81070212）.
文摘Background Skeletal muscle has recently been recognized as an endocrine organ that can express, synthesize and secrete a variety of bioactive molecules which exert significant regulatory effects. Hydrogen sulfide （H2S） iS endogenously produced in mammalian tissues and participates in a number of physiological and pathophysiological processes. We aimed to verify whether H2S could be endogenously generated and released by rat skeletal muscle, and determine the biological effects of H2S in rat skeletal muscle. Methods The study was divided into two parts： detection of endogenous H2S generation and release in rat skeletal muscle and determination of antioxidative activity of skeletal muscle-derived H2S. H2S content and production in tissues were ,detected by sensitive sulfur electrode method. The expressions of H2S producing enzymes cystathionine i^-synthase, cystathionine y-lyase and mercaptopyruvate sulfurtransferase were detected by real-time PCR and western blotting and their tissue distributions were observed by immunohistochemical and immunofluorescent analysis. Rat skeletal muscular ischemia-reperfusion （I-R） injury model was created and evaluated by histological analysis under microscope. The malondialdehyde （MDA） contents, hydrogen peroxide levels, superoxide anion and superoxide dismutase （SOD） activities were detected using spectrophotometer. Results H2S could be endogenously generated and released by skeletal muscle of Sprague-Dawley rats （H2S content： （2.06＋0.43） nmol/mg; H2S production： （0.17＋0.06） nmol.minl.mgl）. Gene and protein expressions of the three H2S producing enzymes ~vere detected in skeletal muscle, as well as the liver and kidney. Endogenous H2S content and production were decreased in skeletal muscles of rats with I-R skeletal muscle injury （P 〈0.05）. Furthermore, H2S significantly protected rat skeletal muscle against I-R injury and resulted in decreased MDA content, reduced hydrogen peroxide and superoxide anion levels, but increased SOD activi
