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目的研究白藜芦醇(resveratrol,Res)对酒精性肝损伤后肝组织氧化反应和炎性反应的影响及与一氧化氮(NO)、诱导型一氧化氮合成酶(iNOS)通路的关系。方法大鼠灌胃给予55度红星二锅头复制肝损伤模型。大鼠随机分为正常对照组、肝损伤模型对照组、Res低剂量组(25 mg.kg-1)、Res中剂量组(50 mg.kg-1)、Res高剂量组(100 mg.kg-1),每日2次,连续7 d。采用试剂盒测定肝脏组织乳酸脱氢酶(LDH)、活性氧(ROS)、还原型谷胱甘肽(GSH)、NO、iNOS和血清IL-10、IFN-γ水平。Western blot测定iNOS表达,RT-PCR测定iNOS mRNA表达。结果与正常对照组相比,酒精性肝损伤模型组肝组织LDH、ROS、NO浓度显著升高(P<0.01)、GSH显著下降(P<0.01),血清IFN-γ水平显著升高、IL-10显著降低(P<0.01),肝组织iNOS和iNOS mRNA表达增加(P<0.01)。与模型组相比,Res显著降低肝脏组织ROS、LDH、NO浓度(P<0.01),降低血清IFN-γ水平和升高血清IL-10与肝脏组织GSH含量(P<0.01),减少iNOS和iNOS mRNA表达(P<0.01)。结论 Res可能通过NO通路,消除氧化性应激状态,改变炎性因子水平,对酒精性肝损伤发挥防治作用。
Objective To investigate the effects of resveratrol (Res) on oxidative and inflammatory responses of liver tissue after alcoholic liver injury and its relationship with nitric oxide (NO) and inducible nitric oxide synthase (iNOS) pathways. Methods Rats were intragastrically given 55 degree red star Erguotou liver injury model. The rats were randomly divided into normal control group, liver injury model control group, Res low dose group (25 mg.kg-1), Res medium dose group (50 mg.kg-1), Res high dose group (100 mg.kg -1) twice daily for 7 days. Lysine dehydrogenase (LDH), reactive oxygen species (ROS), reduced glutathione (GSH), NO, iNOS and serum IL-10, IFN-γ levels in liver tissue were determined by kit. INOS expression was determined by Western blot and iNOS mRNA expression by RT-PCR. Results Compared with the normal control group, the levels of LDH, ROS and NO in liver tissue of alcoholic liver injury model group were significantly increased (P <0.01), GSH was significantly decreased (P <0.01), serum IFN-γ level was significantly increased, IL -10 significantly decreased (P <0.01), the expression of iNOS and iNOS mRNA increased (P <0.01). Compared with the model group, Res significantly decreased the concentrations of ROS, LDH and NO (P <0.01), decreased the level of serum IFN-γ and increased the levels of serum IL-10 and liver GSH (P <0.01) iNOS mRNA expression (P <0.01). Conclusions Res may play a role in prevention and treatment of alcoholic liver injury through NO pathway, eliminating oxidative stress and changing inflammatory cytokines.