红景天甙减轻大鼠酒精性肝损伤

Effect of salidroside on alcohol-injuced hepatic injury in rats

目的:探讨红景天甙对大鼠酒精性肝损伤的作用及其可能机制。方法:将100只SD大鼠随机分为5组:对照组、模型组、联苯双酯滴丸组及红景天甙低剂量(20 mg/kg)和高剂量(40 mg/kg)组,除空白组给予生理盐水外,其余各组均给予56%乙醇灌胃,建立酒精性肝损伤大鼠动物模型,给药组同时予以相应药物灌胃,于末次给药后12 h采血,处死动物后取出肝脏,采用全自动生化仪测定血清甘油三酯(TG)、丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)水平,苏木素-伊红(HE)染色观察肝组织病理学改变,试剂盒测定肝组织中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性,ELISA法测定各组大鼠血清中肿瘤坏死因子α(TNF-α)和核因子κB(NF-κB)水平,Western blot法和RT-PCR测定肝组织TNF-α和NF-κB的蛋白和mRNA表达。结果:与模型组比较,红景天甙高、低剂量组肝组织损伤程度明显减轻;红景天甙对酒精性肝损伤大鼠血清TG、ALT及AST水平均具有明显抑制作用(P<0.05),并可降低肝组织MDA含量,增强肝组织SOD活性(P<0.05);红景天甙各剂量组大鼠血清TNF-α和NF-κB含量降低(P<0.05)。结论:红景天甙能够改善大鼠酒精性肝损伤病理变化,减轻肝组织炎症反应,增加抗氧化酶的活性,降低脂质过氧化,该作用可能与调节NF-κB介导的炎症反应有关。

AIM： To investigate the effect of salidroside on alcoholic hepatic injury in rats. METHODS： The SD rats were randomly divided into 5 groups： negative control group,model group,bifendate group,and low-and highdose salidroside groups. The rats in model group were administered with 56% alcohol,while the rats in negative control group was administered with saline. The rats in bifendate group and salidroside groups were administered with corresponding drugs every day. The blood and the liver tissues were collected to measure triacylglycerol（ TG）,alanine aminotransferase（ ALT）,aspartate aminotransferase（ AST）,malondialdehyde（ MDA） and superoxide dismutase（ SOD）. The pathological changes of the liver tissues were observed with HE staining. Tumor necrosis factor-α（ TNF-α） and nuclear factor-κB（ NF-κB） were measured by ELISA and the protein and mRNA expression levels of TNF-α and NF-κB were detected by Western blot and RT-PCR. RESULTS： Compared with model group,the levels of TG,ALT,AST,MDA,TNF-α and NF-κB were reduced,while the activity of SOD was enhanced in salidroside group（ P〈0. 05）. The liver tissue injury was significantly attenuated. CONCLUSION： Salidroside improves the pathological changes,reduces inflammation,increases the activity of antioxidant enzymes and reduces lipid peroxidation in the liver with alcohol-induced injury. This effect may be related to regulating the NF-κB-mediated inflammatory responses.