论文部分内容阅读
目的:研究甘木通总黄酮(TFCD)对大鼠乳鼠原代心肌细胞缺氧复氧(H/R)损伤的保护作用。方法:采用原代培养SD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、TFCD组(75、150、300μg/m L)及地奥心血康阳性药物对照组。采用MTT法测定TFCD对心肌细胞的存活率;Hoechest染色观察细胞核形态变化;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;荧光法测定细胞内钙离子浓度。结果:TFCD可显著提高H/R损伤心肌细胞内SOD的活性,能显著抑制LDH、CK的活性、MDA的生成以及细胞内钙浓度。结论:TFCD对乳鼠H/R损伤的心肌细胞具有保护作用,其作用机制可能与抗脂质过氧化和减轻细胞内钙超载有关。
AIM: To study the protective effect of total flavonoids of Ganmu tong (TFCD) on hypoxia-reoxygenation (H / R) injury of primary cultured neonatal rat cardiomyocytes. Methods: H / R injury model was established by primary cultured SD rat neonatal rat cardiomyocytes. The experiment was divided into normal group, model group, TFCD group (75,150,300μg / m L) and DIAC positive control group. The survival rate of cardiomyocytes was detected by MTT assay. The morphological changes of nuclei were observed by Hoechest staining. The contents of superoxide dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH) Acid kinase (CK) content; fluorescence determination of intracellular calcium concentration. Results: TFCD significantly increased the activity of SOD in H / R injured myocardium, and significantly inhibited the activities of LDH and CK, the production of MDA and the intracellular calcium concentration. CONCLUSION: TFCD can protect H / R injured cardiomyocytes from neonatal rats, and its mechanism may be related to anti-lipid peroxidation and reducing intracellular calcium overload.