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目的探讨Intermedin(IMD)对大鼠急性心肌缺血再灌注损伤的作用。方法 72只健康雄性SD大鼠随机分为3组:对照组;缺血再灌注组(缺血1h再灌30min);IMD预处理组(缺血再灌注前30min静脉注射10-7mol/L IMD)。检测血清中LDH、心肌中MDA和SOD活性;半定量实时荧光PCR法检测心肌降钙素受体样受体(calcitonin receptor likereceptor,CRLR)、受体活性修饰蛋白(receptor activity modifying protein,RAMP)1/2/3的mRNA表达水平;酶联免疫吸附法(ELISA)测定心肌cAMP含量,SABC法检测Bcl-2/Bax蛋白表达及比值。结果与对照组比较,缺血再灌注组大鼠LDH、MDA分别升高87%和189%,SOD活性下降84%,IMD预处理组LDH、MDA均降低41%,SOD活性升高38%(均P<0.01);实验组心肌CRLR、RAMP1/2/3的mRNA水平均明显上调(P<0.05或P<0.01),与对照组心肌cAMP相比,缺血再灌注组和IMD预处理组分别升高1.36、2.90倍(P<0.05)。Bcl-2/Bax表达比值,缺血再灌注组较对照组降低,IMD预处理组亦低于对照组但高于缺血再灌注组2.225倍。结论 IMD对大鼠急性缺血再灌注损伤的心肌有一定保护作用,减少缺血再灌所致的氧化应激,抑制心肌细胞凋亡可能是其作用机制之一。
Objective To investigate the effect of Intermedin (IMD) on acute myocardial ischemia-reperfusion injury in rats. Methods Seventy-two healthy male Sprague-Dawley rats were randomly divided into three groups: control group, ischemia-reperfusion group (ischemia-reperfusion 30 min), IMD preconditioning group (10-7mol / L IMD ). Serum levels of LDH and MDA and SOD in myocardium were measured. Real-time PCR was used to detect the expressions of calcitonin receptor-like receptor (CRLR), receptor activity modifying protein (RAMP) 1 / 2/3 mRNA expression was detected by enzyme-linked immunosorbent assay (ELISA), and the protein expression and ratio of Bcl-2 / Bax were detected by SABC method. Results Compared with the control group, LDH and MDA increased by 87% and 189% and SOD activity decreased by 84% and 40% respectively in IMD preconditioning group, while the LDH and MDA decreased by 41% and SOD activity increased by 38% (P <0.05 or P <0.01). Compared with the control group, the levels of mRNA of CRLR and RAMP1 / 2/3 in the experimental group were significantly higher than those in the control group Increased by 1.36 and 2.90 times respectively (P <0.05). Bcl-2 / Bax expression ratio, ischemia-reperfusion group decreased compared with the control group, IMD pretreatment group also lower than the control group but higher than the 2.225-fold ischemia-reperfusion group. Conclusion IMD can protect myocardium from acute ischemia-reperfusion injury in rats and reduce oxidative stress induced by ischemia-reperfusion and inhibition of cardiomyocyte apoptosis may be one of its mechanisms.