论文部分内容阅读
目的通过使用盐酸异丙肾上腺素(ISO)制备心肌损伤模型,探讨磷脂酰肌醇3激酶/丝氨酸苏氨酸蛋白激酶(PI3K/AKT)信号通路是否参与心肌损伤的发病机制。方法 20只雄性Wistar大鼠随机分成心肌损伤模型组(ISO组)和对照组。ISO组大鼠每天背部皮下注射ISO 20 mg.kg-1.d-1,对照组大鼠每天注射等量9 g.L-1盐水,均连续注射7 d。采用全自动生化检测仪检测2组大鼠血浆中乳酸脱氢酶(LDH)、肌酸激酶(CK)和α-羟丁酸脱氢酶(α-HBDH)水平。采用蛋白印迹法定量检测大鼠心肌组织中PI3K、p85-PI3K、p55-PI3K、AKT及p-AKT蛋白表达。结果与对照组比较,ISO组大鼠血浆LDH、CK及α-HBDH水平均显著上升,差异有统计学意义(Pa<0.05),证明采用ISO建模成功;与对照组比较,ISO组大鼠心肌组织中PI3K和AKT蛋白水平未见明显变化,但其磷酸化p85-PI3K、p55-PI3K和p-AKT蛋白水平均显著上调,差异有统计学意义(Pa<0.05)。结论在ISO所致的心肌损伤中,PI3K和AKT的磷酸化水平上调,PI3K/AKT信号通路参与ISO所致心肌损伤的发病机制。
Objective To investigate whether PI3K / AKT signaling pathway is involved in the pathogenesis of myocardial injury by using isoproterenol hydrochloride (ISO) to prepare myocardial injury model. Methods Twenty male Wistar rats were randomly divided into myocardial injury model group (ISO group) and control group. The rats in ISO group were injected subcutaneously with ISO 20 mg.kg-1.d-1 every day. The rats in control group were injected with the same amount of 9 g · L-1 saline daily for 7 days. The levels of lactate dehydrogenase (LDH), creatine kinase (CK) and α-hydroxybutyrate dehydrogenase (α-HBDH) in plasma of two groups were detected by automatic biochemical analyzer. Western blotting was used to detect the expression of PI3K, p85-PI3K, p55-PI3K, AKT and p-AKT in rat myocardium. Results Compared with the control group, the levels of plasma LDH, CK and α-HBDH were significantly increased in ISO group (P <0.05), which demonstrated that ISO model was successful. Compared with the control group, ISO group rats PI3K and AKT protein levels in myocardium showed no significant changes, but phosphorylation of p85-PI3K, p55-PI3K and p-AKT protein levels were significantly increased (P <0.05). Conclusions In myocardial injury induced by ISO, the phosphorylation of PI3K and AKT is up-regulated, and the PI3K / AKT signaling pathway is involved in the pathogenesis of myocardial injury induced by ISO.