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目的探讨褪黑素(MT)保护大鼠肝缺血再灌注损伤的机制。方法采取大鼠第一肝门阻断的缺血再灌注模型,将健康雄性SD大鼠64只随机分为两组:对照组和MT组,观察每组动物的病理切片,分别检测血浆丙氨酸氨基转移酶(ALT)、乳酸脱氢酶(LDH)及肝组织匀浆中丙二醛(MDA)、超氧化物歧化酶(SOD)、一氧化氮(NO)的含量,免疫组化测定诱导型NO合酶(iNOS)的表达。结果肝脏缺血再灌注后,有明显的病理损伤改变。MT组再灌注2 h、4 h血清ALT、LDH、肝组织匀浆中MDA和SOD含量与对照组相比均明显降低(均P<0.01),MT组iN-OS表达明显低于对照组(P<0.01)。结论自由基产生过多是肝脏缺血再灌注损伤初期的主要原因,给予MT预处理可通过调节iNOS和SOD来降低MDA、NO水平,从而减轻肝脏损伤。
Objective To investigate the mechanism of melatonin (MT) on hepatic ischemia-reperfusion injury in rats. Methods Sixty-four male Sprague-Dawley rats were randomly divided into two groups: control group and MT group. The pathological sections of each group were observed, and the levels of plasma ammonia The content of malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) in liver, liver, ALT, LDH and immunohistochemistry Inducible nitric oxide synthase (iNOS) expression. Results After liver ischemia-reperfusion, obvious pathological changes were observed. Compared with the control group, the levels of ALT and LDH in serum and the content of MDA and SOD in the liver homogenate of MT group were significantly decreased at 2 and 4 h after reperfusion (all P <0.01), and the expression of iN-OS in MT group was significantly lower than that of the control group P <0.01). Conclusions The excessive production of free radicals is the main reason of liver ischemia-reperfusion injury. Pretreatment with MT can reduce the levels of MDA and NO by regulating the expression of iNOS and SOD, thereby reducing the liver injury.