文献类型：期刊文献

中文题名：金线风总黄酮对四氯化碳致急性肝损伤小鼠的保护作用及机制研究

英文题名：Hepatoprotective Effects and Mechanism of Cyclea hypoglauca( Schauer)Diels Total Flavonoids on Mice with Acute Liver Injury Induced by Carbon Tetrachloride

作者：葸博婷[1];钟明利[1];曹后康[1];管玉满[1];陈毅飞[1];晋玲[2];张可锋[1,2]

第一作者：葸博婷

机构：[1]桂林医学院,桂林541004;[2]甘肃中医药大学,兰州730000

第一机构：桂林医学院,桂林541004

年份：2018

卷号：30

期号：7

起止页码：1208

中文期刊名：天然产物研究与开发

外文期刊名：Natural Product Research and Development

收录：CSTPCD;;北大核心:【北大核心2017】；CSCD:【CSCD2017_2018】；

基金：广西八桂学者专项项目(桂财教函[2017]143号)

语种：中文

中文关键词：金线风;总黄酮;急性肝损伤;氧化应激;炎症反应;TLR-4/NF-κB信号通路

外文关键词：Cyclea hypoglauca （Schauer） Diels;total flavonoids;acute liver injury-;oxidative stress;inflammatory response;toll-like receptor-4/nuclear factor-kappa B pathway

摘要：研究金线风总黄酮(TFC)对四氯化碳(CCl4)致急性肝损伤小鼠的保护作用,并从氧化应激、炎症反应和TLR-4/NF-κB信号通路探讨其作用机制。60只小鼠随机分为正常组、模型组、水飞蓟素组(150 mg/kg)、TFC低、中、高剂量组(100、200、400 mg/kg)、连续灌胃给药10 d。末次给药2 h后,除正常组外,各组腹腔注射0.1%的CCl4花生油溶液(10 m L/kg),建立小鼠急性肝损伤模型,16 h后,收集血清和肝组织。血清指标检测表明,与模型组比较,TFC能够显著降低肝脏指数、ALT和AST活性(P<0.05),并减少ALP、TBIL和γ-GT含量(P<0.05),且降低MDA含量(P<0.05),同时增强T-SOD和GSH-Px活性(P<0.05)。ELISA法检测肝组织指标结果表明,与模型组比较,TFC能够显著下调TNF-α、IL-1β和IL-6含量(P<0.05)。Western blot检测结果显示,与模型组比较,TFC能够明显降低肝组织中TLR-4和NF-κB蛋白表达(P<0.05)。HE染色分析肝组织病理学变化结果表明,TFC能够有效改善肝组织损伤程度。综上所述,TFC对CCl4诱导的急性肝损伤小鼠具有保护作用,其保肝作用机理可能与抑制氧化应激、炎症反应以及TLR-4/NF-κB信号通路有关。
To study the hepatoprotective effects of the total flavonoids extracted from the dried root of Cyclea hypoglauca（ Schauer） Diels（ TFC） on mice with acute liver injury induced by carbon tetrachloride（ CCl4）,and explore the mechanism based on oxidative stress,inflammatory response and toll-like receptor-4（ TLR-4）/nuclear factor-kappa B（ NF-κB）pathway. 60 mice were randomly divided into normal group,model group,silymarin group（ 150 mg/kg）,and TFC-low,medium,high dose groups（ 100,200,400 mg/kg）. All mice were administrated by gavage once a day for 10 d with distilled water or corresponding dose of drugs（ 10 m L/kg）. After 2 h of the last administration,the mice were injected intraperitoneally with 0. 1% CCl4 peanut oil solution（ 10 m L/kg） to induce the acute liver injury except the normal group. 16 h later,the eye balls of mice were removed to take blood,and all mice were sacrificed to collect the liver tissue. Liver index was calculated based on body weight and liver weight of mice. Biochemical methods were used to measure the serum contents of alanine aminotransferase（ ALT）,aspartate aminotransferase（ AST）,alkaline phosphatasetotal（ ALP）,total bilirubin（ TBIL）,γ-glutamyl transpeptidase（ γ-GT）,superoxide dismutase（ T-SOD）,malondialdehyde（ MDA） and glutathione peroxidase（ GSH-Px）. The enzyme-linked immunosorbent assay（ ELISA） was used to detect the hepatic levels of tumor necrosis factor-α（ TNF-α）,interleukin-1β（ IL-1β） and interleukin-6（ IL-6）. The relative expressions of TLR-4 and NF-κB in liver tissue were detected by Western blot. HE staining was used to observe the histopathological changes ofliver. The results showed that TFC could significantly improve the liver tissue lesion,decrease the liver index and serum contents of AST,ALT,ALP,TBIL,γ-GT and MDA（ P〈0. 05）,enhance the activity of T-SOD and GSH-Px（ P〈0. 05）,and inhibit the hepatic levels of TNF-α,IL-1β,IL-6,TLR-4 and NF-κB（ P〈0. 05）. In summary,TFC had a hepatoprotective effect on mice with acute liver injury induced by CCl4,and its mechanism may be related to inhibiting the oxidative stress levels,inflammatory response and TLR-4/NF-κB pathway.