AIM: To explore the protective effect of riboflavin preconditioning on hepatic ischemia/reperfusion injury in rats. METHODS: Twenty - four Sprague - Dawley rats were randomly divided into 3 groups ( n = 8 ): sham group, ischemia/reperfusion ( I/R ) group and riboflavin preconditioning ( R + I/R ) group. The rats in sham group and I/R group received a standard chow, while the rats in R + I/R group received a chow supplemented with riboflavin. After 4 weeks, portal vein and hepatic artery supplying the middle and left hepatic lobes were clamped with a traumatic vascular clip for induction of partial hepatic ischemia in the rats in I/R group and R + I/R group. After 1 h of ischemia, 1 h of reperfusion was conducted by removal of the clip. The activity of alanine aminotransferase ( ALT ) and aspartate aminotrans-ferase ( AST ) in serum, the activity of superoxide dismutase ( SOD ) and the level of malondialdehyde ( MDA ) in serum and liver were measured. Western blotting was employed to examine the protein expression of heme oxygenase -1( HO - 1 ) in the liver. RESULTS: The results showed that ischemia/reperfusion injury markedly increased the activity of AST and ALT in serum, decreased the activity of SOD, and elevated the level of MDA and the activity of HO ?1 in the liver as compared with sham group ( P <0. 01 ). The riboflavin pretreatment significantly decreased the activity of AST and ALT in serum, increased the activity of SOD and decreased the levels of MDA in serum and liver as compared with I/R group ( P <0. 01 ). In addition, the protein expression of HO - 1 and the activity of HO - 1 were elevated in R + I/R group ( P <0. 01 ). Cyto-plasmic vacuolation and swelling of the hepatocytes were observed in I/R group. Treatment with riboflavin markedly alleviated the changes of liver structure. CONCLUSION: Riboflavin preconditioning has protective effect on hepatic ischemia/ reperfusion injury. The mechanism may be correlated with enhancing the anti - oxidation and alleviating the reaction of lipid peroxidation.%目的:探讨核黄素对肝缺血再灌注损伤的影响及其机制.方法:将24只SD大鼠随机分为3组,每组8只.假手术对照组(sham组)和缺血再灌注组(I/R组)大鼠喂以正常饲料,核黄素预处理组(R+I/R组)大鼠补充核黄素.喂养4周后,阻断大鼠肝门1 h,再灌注1 h建立I/R模型.术后采血并收集肝脏标本,分别检测血清及肝组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)水平和血清丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)的活性;蛋白印迹法检测肝组织血红素加氧酶-1(HO-1) 表达情况;HE染色观察肝组织病理学改变.结果:与sham组比较,I/R组大鼠血清AST、ALT活性及MDA水平均明显升高,SOD活性显著降低(P<0.01);肝组织中SOD活性亦明显下降(P<0.01),MDA水平及HO-1蛋白表达则显著增高(P<0.05).而R+I/R组较I/R组大鼠血清AST、ALT活性及MDA水平均明显下降,SOD活性显著增强(P<0.01);肝组织中MDA水平亦明显降低,SOD及HO-1蛋白表达显著增高(P<0.01).组织切片显示I/R组大鼠肝细胞肿胀,炎症细胞浸润,小叶结构紊乱;R+I/R组大鼠肝细胞仅轻度肿胀,几乎无气球样变,小叶结构清晰.结论:核黄素预处理对缺血再灌注肝脏具有显著的保护作用,其作用机制可能与核黄素通过降低MDA水平、提高SOD活性及HO-1蛋白表达,增强肝脏的抗氧化能力,减轻脂质过氧化反应有关.
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