+-K+-ATP酶、Ca2+-Mg2+-ATP酶活性。結(jié)果 與模型組(42.60%)比較,丹酚酸B高、低劑量組的MIA分別縮小至35.93%和37.21%,差異顯著(P<0.05);與模型組比較,丹酚酸B高、低劑量組血清CK、LDH活力均顯著降低(P<0.05、0.01);與模型組比較,丹酚酸B高、低劑量組心肌組織Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶活性均顯著升高(P<0.05、0.01)。結(jié)論 丹酚酸B預(yù)處理可保護(hù)MI/RI所致心肌損傷,作用途徑可能與改善心肌組織的能量代謝相關(guān)。;Objective To investigate the effects of Salvianolic acid B (Sal B) pretreatment against myocardial ischemia/reperfusion injury (MI/RI) in rats. Methods MI/RI rats model was established by 30 min of coronary artery ligation and subsequent 2 h of reperfusion. Rats were randomly divided into four groups (n=10):sham group, model group, and Sal B low (10 mg/kg) and high dose (20 mg/kg) group. Before the modeling operation, Sal B was injected intraperitoneal once daily for 7 d. After the modeling operation, the activities of creatine kinase (CK) and lactate dehydrogenase (LDH) in serum of rats were detected by chromatometry, myocardial infarction area (MIA) in rats were examined by staining method and Na+-K+-ATPase and Ca2+-Mg2+-ATPase activities in myocardial tissues were determined by phosphorus method. Results Compared with model group, high and low doses of Sal B significantly reduced MIA to 35.93% and 37.21%, respectively (P<0.05). Compared with model group, the activities of serum CK and LDH activities in Sal B high and low dose groups were significantly decreased (P<0.05, 0.01); Compared with model group, the activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase in myocardium of Sal B high and low dose groups were significantly increased (P<0.05 and 0.01). Conclusion Sal B pretreatment could protect MI/RI, and its effects maybe related with the improvement of myocardial energy metabolism."/> +-K+-ATP酶;Ca2+-Mg2+-ATP酶;Salvianolic acid B;myocardial ischemia/reperfusion injury;Rat;energy metabolism"/>

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首頁(yè) > 過(guò)刊瀏覽>2018年第41卷第12期 >2018,41(12):2210-2213. DOI:10.7501/j.issn.1674-6376.2018.12.014
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丹酚酸B預(yù)處理對(duì)心肌缺血/再灌注損傷能量代謝的影響

Salvianolic acid B pretreatment protects myocardial ischemia/reperfusion injury through improvement of energy metabolism

發(fā)布日期:2018-12-17
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