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苦丁茶多酚提取物对四氯化碳诱导小鼠肝损伤的改善作用及机制研究
引用本文:赵欣,李贵节,胡园园,易若琨,宋家乐.苦丁茶多酚提取物对四氯化碳诱导小鼠肝损伤的改善作用及机制研究[J].食品工业科技,2018,39(4):289-295.
作者姓名:赵欣  李贵节  胡园园  易若琨  宋家乐
作者单位:1. 重庆第二师范学院, 重庆市功能性食品协同创新中心, 重庆市功能性食品工程技术研究中心, 功能性食品研发重庆市工程实验室, 生物与化学工程学院, 重庆 400067;2. 桂林医学院公共卫生学院食品卫生与营养学教研室, 广西高校预防医学重点实验室, 广西桂林 541004
基金项目:重庆第二师范学院引进高层次人才项目(2013BSRC001)。重庆高校创新团队建设计划资助项目(CXTD201601040)
摘    要:本文研究苦丁茶多酚提取物(PEK)对小鼠肝损伤的改善效果。通过腹腔注射CCl4诱导小鼠肝损伤,采用苦丁茶多酚提取物(PEK)灌胃昆明小鼠,对小鼠的血清和肝组织的mRNA表达进行了检测。结果显示,PEK中多酚物质的含量为71.3%。与模型组相比,PEK能够显著降低CCl4诱导肝损伤小鼠的肝指数和血清中天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、碱性磷酸酶(ALP)、甘油三酯(TG)、总胆固醇(TC)、尿素氮(BUN)、一氧化氮(NO)和丙二醛(MDA)水平,提高白蛋白(ALB)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)水平;PEK还能够显著降低肝损伤小鼠血清中白细胞介素-6(IL-6)、白细胞介素-12(IL-12)、肿瘤坏死因子α(TNF-α)和γ-干扰素(IFN-γ)细胞因子含量(p<0.05)。病理学观察表明,PEK能够有效地降低CCl4造成肝组织形态不完整和肝细胞坏死。逆转录聚合酶链式反应(RT-PCR)实验结果表明,PEK能够显著上调小鼠肝组织中锰超氧化物歧化酶(Mn-SOD)、铜锌超氧化物歧化酶(Gu/Zn-SOD)、CAT、GSH-Px等抗氧化酶的mRNA表达和下调环氧化酶2(COX-2)、白细胞介素-1β(IL-1β)、TNF-α表达(p<0.05)。由此可见,PEK是一类具有肝损伤改善作用的活性成分,具有较好的应用前景。

关 键 词:苦丁茶    多酚提取物    肝损伤    四氯化碳
收稿时间:2017-06-26

Improvement effects and mechanism research of polyphenol extracts from Kudingcha on carbon tetrachloride induced hepatic damage in mice
ZHAO Xin,LI Gui-jie,HU Yuan-yuan,YI Run-kun,SONG Jia-le.Improvement effects and mechanism research of polyphenol extracts from Kudingcha on carbon tetrachloride induced hepatic damage in mice[J].Science and Technology of Food Industry,2018,39(4):289-295.
Authors:ZHAO Xin  LI Gui-jie  HU Yuan-yuan  YI Run-kun  SONG Jia-le
Abstract:The improvement effects of polyphenol extracts of kudingcha(PEK)on hepatic damage in mice were determined in this study. The mice were fed with PEK by gavage,and through the mice were induced hepatic damage using CCl4 by intraperitoneal injection,the serum and mRNA expression of hepatic tissue in mice were measured. The results showed that the polyphenol contents of PEK was 71.3%. PEK could reduce the liver index of CCl4-treated mice as compared to the control group,meanwhile,and PEK also could significantly reduce the serum AST,ALT,ALP,TG,TC,BUN,NO,MDA levels and raise SOD,CAT,GSH-Px levels(p<0.05). PEK also could significantly decrease serum cytokine IL-6,IL-12,TNF-α and IFN-γ levels in gastric injury mice(p<0.05). Pathological observation also showed that PEK could effectively reduce the hepatic tissue destruction and hepatocellular necrosis caused by CCl4. The RT-PCR experiment results showed that PEK could significantly increase Mn-SOD,Gu/Zn-SOD,CAT,GSH-Px mRNA expressions and decrease COX-2,IL-1β,TNF-α expressions of hepatic tissues in mice compared to the mice in control group(p<0.05). It could be seen that PEK is a kind of active component with improving liver injury,therefore it has a good application prospect.
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