柚皮苷对抗表阿霉素所致H9C2心肌细胞毒性的研究

To explore the clinical value of naringin’s protective effect againstepirubicin induced H9C2 cardiomyocyte toxicity

目的:柚皮苷(Nar)对抗表阿霉素(EPI)所致H9C2心肌细胞毒性的研究。方法:取H9C2心肌细胞均分为空白组、对照组、模型组、低剂量、中剂量及高剂量组,低剂量、中剂量及高剂量组分别给予10,20,40μmol·L^(-1)Nar预处理24 h后加入5μmol·L^(-1)EPI,对照组加入等体积的培养基,同样条件下培养。ELSIA法检测5组细胞肌酸激酶同工酶(creatine kinase-MB,CK-MB)、乳酸脱氢酶(LDH)、丙二醛(MDA)水平,CCK-8法检测5组心肌细胞活力,Western blot法检测GRP78、Bax及Bcl-2蛋白水平。结果:(1)CK-MB、LDH及MDA水平在模型组>低剂量组>中剂量组>高剂量组>对照组,差异均有统计学意义(均为P<0.05);(2)心肌细胞活力在对照组>高剂量组/中剂量组>低剂量组>模型组,差异均有统计学意义(均为P<0.05),但高剂量组及中剂量组间无统计学意义(P>0.05);(3)GRP78及Bax蛋白水平在模型组>低剂量组>中剂量组/高剂量组>对照组,但Bcl-2蛋白水平在对照组>高剂量组/中剂量组>低剂量组/模型组,差异均有统计学意义(均为P<0.05)。结论:柚皮苷具备潜在的保护表阿霉素所致H9C2心肌细胞损伤作用,其作用机制可能与上调Bcl-2表达有关。

OBJECTIVE To explore the protective effectof naringin against epirubicin(EPI)induced H9 C2 cardiomyocyte toxicity.METHODS H9 C2 cardiomyocytes with logarithmic growth cycle were divided into control group,model group,low-dose,middle-dose and high-dose experimental groups.The low-dose,middle-dose and high-dose experimental groups were given 10,20 and 40 μmol·L^(-1),respectively Nar was pretreated for 24 h,5 μmol·L^(-1)EPI was added in addition to the normal group,and five groups of cell creatine kinase-MB(CK-MB),lactic acid dehydrogenase(LDH)and malonaldehyde(MDA)were detected by ELSIA,CCK-8 was used to detect the viability of five groups of cardiomyocytes,Western blot was used to detect GRP78,Bax and Bcl-2 protein.RESULTS The levels of CK-MB,LDH and MDA in model group>experimental-L>experimental-H>control group,all of P values were less than 0.05;myocardial cell viability in control group> experimental-H/experimental-M group> experimental-L group> model group,all of P values were less than 0.05;levels of GRP78 and Bax protein in model group>experimental-L group> experimental-M/experimental-H group>control group,while levels of Bcl-2 protein in control group> experimental-H/experimental-M group> experiment-L/model group,all of P values were less than 0.05.CONCLUSION Naringin plays a protective role in cardiomyocyte damage induced by EPI through up-regulation of Bcl-2 expression.