β-细辛醚对阿霉素诱导乳鼠心肌细胞损伤的影响

目的:探讨β-细辛醚对阿霉素(ADR)所致心肌细胞损伤的保护作用及机制.方法:分离培养出生1～3d大鼠心肌细胞,随机分为正常对照组、ADR(2.0 mg·L-1)模型组、β-细辛醚(10,20,40 mg·L-1)剂量组.72 h后,观察心肌细胞形态及搏动频率,MTT比色法检测细胞存活率,试剂盒检测培养基中乳酸脱氢酶(LDH)含量、超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量,免疫组织化学法检测B细胞淋巴瘤/白血病-2(Bcl-2),Bel-2相关蛋白(Bax)表达.结果:与正常对照组比较,ADR模型组心肌细胞皱缩变形,不规则,细胞间隙变大,搏动节律不齐,频率明显减慢;心肌细胞存活率明显减少;LDH漏出量增加;SOD活力降低;MDA含量增高;Bcl-2蛋白表达降低、Bax蛋白表达增高(P＜0.01或P＜0.05).与ADR模型组比较,β-细辛醚各剂量组心肌细胞形态较规则,细胞搏动频率规则、增高,呈现向心性同步化搏动;心肌细胞存活率明显增高;LDH漏出量降低;SOD活力增高;MDA含量降低;Bcl-2蛋白表达增高、Bax蛋白表达降低(P＜0.01或P＜0.05).结论:β-细辛醚对阿霉素诱导心肌细胞损伤具有保护作用,其机制可能与抗自由基,减轻脂质过氧化及抑制细胞凋亡有关.

Effect of Beta-asarone on Adriamycin-induced Cardiomyocyte Injury in Suckling Mouse

Objective: To observe the effect of beta-asarone on adriamycin-induced cardiomyocyte injury in suckling mouse. Method: Cardiomyocytes of neonate rat were cultivated for 72 hours and randomly divided into normal control group, adriamycin(ADR,2 mg·L^-1) model group,and beta-asarone(10,20,40 mg·L^-1) dose groups. MTT colorimetric method was deployed to detect cardiocyte survival rate,activities of medium lactate dehydrogenase(LDH), superoxide dismutase(SOD) and malondialdehyde(MDA) were detected,and protein expression of B cell lymphoma/lewkmia-2(Bcl-2) and Bcl-2 associated X protein(Bax) were detected by immune histochemical method. Result: Compared with normal control group, model group ADR cardiomyocyte shrinkage deformation,irregular,beat rhythm irregularities,frequency obviously slow down, numbers of survival cells were decreased, the leakage of LDH was increased; SOD activity was decreased; the contents of MDA were increased; protein expressions of Bcl-2 were reduce, protein expressions of Bax were increased (P <0.01 or P <0.05). And compared with ADR model groupand ADR model group, each dose group of beta-asarone had no changes in cardiomyocytes cell pulsation frequency, present centrality synchronization pulsing; cardiomyocytes survival rate was increased; the leakages of LDH was decreased;and the activity of SOD was increased; contents of LDH and MDA were decreased; protein expression of Bcl-2 was increased, protein expression of Bax were reduced (P<0.01 or P <0.05). Conclusion: Beta-asarone protects mice from adriamycin-induced cardio-toxicity by reduction of oxygen free radicals and apoptosis in mouse cardiac tissues.