黄芪多糖对乳鼠心肌细胞缺氧/复氧损伤的保护作用

目的探讨黄芪多糖(APS)对乳大鼠培养心肌细胞缺氧/复氧损伤的保护作用及其机制。方法取体外培养的乳大鼠心肌细胞建立缺氧/复氧心肌细胞损伤模型,实验分为5组:空白对照组;模型组(A/R组);3个APS给药组,于缺氧及复氧开始时分别加入终浓度为10、30、100mg·mL-1的APS,观察APS对细胞上清液中缺氧/复氧后LDH、CK、AST漏出量、MDA含量、SOD活性。用MTT法检测APS对缺氧/复氧损伤心肌细胞存活率的影响。用流式细胞仪测定APS对缺氧/复氧损伤心肌细胞凋亡的影响。结果 APS可明显减少缺氧/复氧后LDH、CK、AST漏出量(P<0.05或P<0.01);降低MDA含量,提高SOD活性(P<0.05或P<0.01);明显提高缺氧/复氧损伤心肌细胞的存活率,并能明显抑制缺氧/复氧损伤心肌细胞凋亡。结论 APS对培养心肌细胞的缺氧/复氧损伤具有保护作用,作用机制与其增强细胞抗氧化作用,减少自由基及脂质过氧化物导致的细胞膜损伤和抑制细胞凋亡有关。

Protective effects of Astragalus Polysaccharide on cultured myocardial cells subjected to anoxia/reoxygenation injury in neonatal rats

Aim To study the protective effects of Astragalus Polysaccharide(APS)on myocardial cells injured by anoxia/reoxygenation(A/R)in neonatal rats.Methods An anoxia/reoxygenation model of myocardial cells from neonatal Sprague Dawley(SD)rats was established.The cells were randomly divided into 5 groups:blank control group;A/R group;A/R+APS(10,30,100 mg·L-1)groups.APS was added into the culture medium with a final concentration 10,30,100 mg·L-1 before anoxia and reoxygenation.Lactate dehydrogenase(LDH),Cmatine kinase(CK)and Aspartate aminotransferase(AST)release,Malondialdehyde(MDA)contents and Superoxide dismutase(SOD)activity in the bathing medium were assayed for the evaluation of myocardial cells injury.The protective role of APS in mitochondria of myocardial cells was measured by MTT after A/R injury.Cardiomyocyte apoptosis was detected by flow eytometry.Results APS could restrain the LDH,CK and AST release evidently,decrease the MDA content and enhance the SOD activity,increase OD490 of myocardial cells injured by A/R and inhibit cardiomyocyte apoptosis.Conclusion APS can produce effect of protecting the cultured myocardial cells injured by A/R.The mechanism is related to the enhancement of antioxidative effect on cells,and the reduction membrane damage caused by free radical and lipid peroxide,and inhibit cardiomyocyte apoptosis.