摘要
目的探讨褪黑素对大鼠肝缺血再灌注损伤的保护作用及其机制。方法将72只6―7周龄的健康雄性Wistar大鼠,随机分为3组,即褪黑素处理组(Mel组)、酒精溶媒对照组(Alc组)、生理盐水对照组(NS组)。建立肝缺血再灌注损伤模型,于不同时点用TBA法和黄嘌呤氧化酶法分别测定肝组织丙二醛(MDA)及超氧化物歧化酶(SOD)含量,免疫组织化学方法检测分析核因子-κB(NF-κB)的表达情况,结果MDA含量在再灌注后各时点的Mel组均显著低于Alc及NS对照组(P<0.05),SOD含量在再灌注后3h、12h、24h时点的Mel组显著高于Alc及NS对照组(P<0.05);Mel组再灌注后各时点的NF-κB蛋白表达阳性率均显著低于Alc组和NS组(P<0.05)。以上各项指标在各时点Alc组与NS组相比无显著性差异。结论Mel抗氧化及抑制肝细胞NF-κB的表达,可能是大鼠肝缺血再灌注损伤的保护作用机制之一。
Objective To explore the protective effect and mechanism of melatonin (Mel) on rat's hepatic iscbemia-reperfusion injury. Methods 72 healthy male Wistar rats 46-7 weeks old ) were randomly divided into 3 groups: Mel treated group (Mel), alcohol solvent control group (Alc) and saline control group (NS). To establish partial hepatic ischemia-reperfusion injury models, malonaldehyde (MDA) , superoxide dismutase (SOD) were examined by TBA method and xanthinoxidase method respectively,immunohistochemistry stainning was used to detect the expression of naclear factor (NF- kB). Results The level of MDA in Mel group was significantly lower than that in the Alc and NS groups (P〈0.05), the level of SOD of Mel group measured in 3h, 12h, 24h after reperfuslon was significantly higher than that in Alc and NS groups (P〈0.05). The expression of NF-kB in Mel group markedly lower than that in Alc and NS groups (P〈0.05). Without significant differences between Alc and NS group. Conclusion The inhibition of the expression of NF- kB by Mel may be one of the mechanisms for the protective effect of Mel on hepatic ischemia-reperfusion injury.
出处
《解剖科学进展》
CAS
2007年第2期121-123,共3页
Progress of Anatomical Sciences