绿茶多酚对实验性酒精性肝损伤大鼠的治疗作用  

Effects of tea polyphenols on alcoholic liver injury in rats

作　　者：周晓蓉[1] 龚作炯[1] 袁光金[1] 张频[1] 

机构地区：[1]武汉大学人民医院感染科,湖北省武汉市430060

出　　处：《世界华人消化杂志》2006年第1期50-56,共7页World Chinese Journal of Digestology

摘　　要：目的:研究绿茶多酚及表没食子儿茶素没食子酸酯(EGCG)对大鼠酒精性肝损伤的治疗作用,并探讨其作用机制.方法:将48只大鼠随机分为正常对照组、模型组、茶多酚治疗Ⅰ组、Ⅱ组、EGCG治疗Ⅰ组、Ⅱ组,每组8只大鼠.以酒精+0.5mL鱼油灌胃制作酒精性肝病模型.茶多酚治疗Ⅰ、Ⅱ组另外分别给予200mg/kg、100mg/kg茶多酚灌胃治疗,EGCGⅠ、Ⅱ治疗组则分别给予100mg/kg、50mg/kgEGCG灌胃治疗.5wk后处死大鼠,观察各组大鼠肝脏病理变化,并测定血清转氨酶及血浆内毒素水平,采用ELISA法检测血清TNF-α、IL-1、IL-18水平,并应用RT-PCR方法检测大鼠肝组织CD14、LBP、TNF-α、IL-1、IL-18mRNA的表达,并应用图像分析系统对其进行半定量分析.结果:模型组大鼠肝组织表现肝细胞中度脂肪变性,点状坏死,炎性细胞浸润,其血清ALT、TNF-α、IL-1、IL-18及血浆内毒素水平与正常对照组相比,显著升高(P<0.05或P<0.01);模型组肝组织CD14、LBP、TNF-α、IL-1、IL-18mRNA的表达与对照组相比显著增强(P<0.05或P<0.01).茶多酚、EGCG高低剂量分别同时处理显著降低了酒精性肝损伤大鼠血清ALT、TNF-α、IL-1、IL-18与血浆内毒素水平及肝组织CD14、LBP、TNF-α、IL-1、IL-18mRNA的表达(P<0.05或P<0.01),肝组织仍可见肝细胞脂肪变性,但未见坏死及炎性细胞浸润.结论:茶多酚及EGCG可减轻酒精性肝损伤大鼠肝脏的炎症与坏死,其可能机制包括降低内毒素血症,抑制Kupffer细胞活性与促炎细胞因子的表达与分泌.AIM： To investigate the effects of tea polythenols （TP） and epigallocatechin-3-gallate （EGCG） on alcohol-induced liver injury in rats. METHODS： Forty-eight Sprague-Dawley rats were randomly divided into normal control, model, TP treatment （100, 200 mg/kg）, and EGCG treatment （50, 100 mg/kg） groups. Alcoholic liver injury was induced by ethanol plus 0.5 mL fish oil intragastically for 5 wk. Liver injury was assessed by pathological examination and serum alanine aminotransferase （ALT） levels. The plasma endotoxin and serum tumor necrosis factor（TNF）-α, interleukin（IL）-1 and IL-18 levels were measured by enzyme linked immunosorbent assay （ELISA）. The expression of CD14, lipopolysaccharide-binding protein （LBP）, TNF-α, IL-1 and IL-18 mRNA in the liver were detected by reverse transcription chain reaction （RT-PCR）. RESULTS： Chronic intragastric irrigation of alcohol plus fish oil resulted in the elevated serum ALT, fatty degeneration, focal necrosis and inflammatory cell infiltration in the liver of model rats. These changes were accompanied by increased plasma endotoxin and serum TNF-α, IL-1, IL-18 levels （P 〈 0.05 or P 〈 0.01）. The expression of CD14, LBP, TNF-α, IL-1, and IL-18 mRNA was also increased in the model rats. However, TP and EGCG treatment improved histological changes, and significantly decreased the levels of plasma endotoxin and serum TNF-α, IL-1, IL-18, as well as the expression of CD14, LBP, TNF-α, IL-1 and IL-18 mRNA （P 〈 0.05 or P 〈 0.01）. Fatty degeneration was still observed in TP and EGCG treatment group, but focal necrosis and inflammatory cell infiltration disappeared. CONCLUSION： TP and EGCG can protect liver against necrosis and inflammation induced by alcohol, and the mechanism may involve its effect on the reduction of plasma endotoxia, and inhibition of Kupffer cell activity and proinflammatory cytokine expression and secretion.

关 键 词：酒精性肝病 茶多酚 EGCG 内毒素血症 细胞因子 

分 类 号：R285.5[医药卫生—中药学]