β-细辛醚对阿霉素诱导乳鼠心肌细胞损伤的影响

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

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1～3 d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。

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; contentsof 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.