葛根素对缺氧再复氧心肌细胞损伤的保护作用

Protective effects of puerarin on cardiomyocytes from hypoxia/reoxygenation injury

目的观察葛根素对缺氧再复氧心肌细胞损伤的保护作用,探讨其保护作用的可能机制。方法将原代培养的新生大鼠心肌细胞分成2组:缺氧再复氧(hypoxia/reoxygenation,H/R)对照组和缺氧再复氧+葛根素(puerar-in)保护组。葛根素浓度分别用200μmol/L、100μmol/L、50μmol/L。检测两组心肌细胞存活率(V iab ility)、培养基中乳酸脱氢酶(lactate dehydrogenase,LDH)活性、肌酸激酶(creatine k inase,CK)活性以及心肌细胞Ca2+浓度、超氧物歧化酶活性(superoxide d ismutase,SOD)和丙二醛(m alond ial dehyde,MDA)含量。结果缺氧再复氧造成心肌细胞存活率显著降低(P<0.01),LDH和CK外泄;而葛根素处理能显著提高细胞存活率(P<0.01),显著减少LDH和CK外泄(P<0.01)。同时各葛根素处理组心肌细胞SOD活性显著高于对照组(P<0.01),而Ca2+和MDA含量则显著低于对照组(P<0.01)。结论葛根素对缺氧再复氧心肌细胞损伤有明显的保护作用,其保护效应的机制可能与葛根素抑制心肌细胞Ca2+超载、保护心肌细胞SOD活性、防止细胞膜过氧化作用有关。

Objective To observe protective effects of puerarin on cardiomyocytes suffering from hypoxia/ reoxygenation injury and to discuss the possible mechanism of cardiomyocyte injury protect. Methods Primary cultured cardiomyocytes of neonatal SD rats were randomly divided into 2 groups: the hypoxia/ reoxygenation(H/ R,control) group and the puerarin group(cardiomyocytes suffering from hypoxia/ reoxygenation were treated with 200μmol/ L,100μmol/ L,50μmol/ L of puerarin).The following parameters of the two groups were determined: cardiomyocyte viability,lactate dehydrogenase(LDH) activity,creating kinase(CK) activity,intracellular superoxide dismutase(SOD) activity,calcium concentration and malondialdehyde(MDA) content. Results Following H/ R,cardiomyocytes were heavily injured and cell viability declined with LDH and CK leakage;In comparison with those in the control group,puerarin could increase cardiomyocyte viability(P<0.01) and reduce LDH and CK leakage(P<0.01).After H/ R,SOD activity of cardiomyocytes in the puerarin group was obviously higher than that in control group;while both calcium concentration and MDA content in cardiomyocytes in the puerarin group were obviously lower than those in the control group(P<0.01). Conclusion Puerarin has a remarkable protective effect on cardiomyocytes suffering from hypoxia/ reoxygenation injury by mechanisms of prohibiting calcium overload of cardiomyocytes,keeping SOD activity and protecting cell membrance from over oxidation.