香青兰总黄酮抗心肌细胞缺氧/复氧损伤作用的研究

为研究香青兰总黄酮对体外培养心肌细胞缺氧/复氧(H/R)损伤的保护作用及其机制。采用体外原代培养Wistar大鼠乳鼠心肌细胞建立H/R损伤模型,实验分为正常组、模型组、香青兰总黄酮高、中、低剂量组及丹参滴丸阳性药物对照组。采用MTT法测定香青兰总黄酮对心肌细胞的毒性作用;比色法测定培养液中超氧化物歧化酶(SOD)、丙二醛(MDA)、乳酸脱氢酶(LDH)、肌酸激酶(CK)的含量;HE染色法检测细胞形态;免疫组化法测定Bcl-2、Bax蛋白表达。结果表明,香青兰总黄酮各给药组均能降低心肌细胞损伤程度,与模型组比较,香青兰总黄酮高、中剂量组均能够明显降低MDA含量(P0.01,P0.05),降低LDH释放量(P0.01,P0.05),增加Bcl-2表达,减少Bax表达;香青兰总黄酮高剂量组可以提高SOD活性(P0.01),降低CK释放量(P0.05)。香青兰总黄酮对大鼠心肌细胞H/R损伤有保护作用,其作用机制可能与清除氧自由基和调节凋亡蛋白的表达有关。

Protective Effects of Dracocephalum moldavica L.Flavonoids on Cultured Cardiomyocytes in Vitro Hypoxia/Reoxygenation

To explore the protective effect of Draeocephalum Moldavica L.Flavonoids on cultured cardiomyocytes in vitro hypaxia /reoxygenation （H/R）.Primary culture of Wistar Rat cardiomyocytes in vitro and randomized to normal group, model group, dracocephalum moldavica flavonoids groups with high, middle, and low dose, and positive drug group, according to different interventions.MTr assay was used to detect the toxic effect of Dracocepbalum Moldavica L. Flavonoids on myocardial viability. Cell supernatant was collected and determinated the Super oxides differences of enzyme （SOD）,Malondialdehyde （MDA）,lactate dehydrogenase （LDH）,and ereatine kinase （CK）.Cell modality was detected by HE staining, Bcl-2,and Bax protein expression were determined through immunohistochemisty.All groups of Dracocephalum Moldavica L.Flavonoids could reduce the degree of cardiomyocytes injury compared with the model groups.High and middle dosage of a Dracocephalum Moldavica L.Flavonoids significantly reduced MDA concentration （P〈0.01,P〈0.05）,reduced LDH level （P〈0.01,P〈0.05）,increased the expression of Bcl-2 and decreased the expression of Bax protein expression compared with the model group.High dosage of Dracocephalum moldavica L.Flavonoids increased SOD activity （P〈0.01）,and reduced CK level （P〈0.05）.Dracocephalum Moldaviea L.Flavonoids could protect rats cardiomyocytes from hypoxia-reoxygenation injury,the mechanism may relate to influence the expression of apoptotic protein and remove oxygen free radicals.