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青藤碱缓解氧化应激和炎症反应对四氯化碳诱导的急性肝损伤小鼠的保护作用
引用本文:郭 华  裴高油  李龙腾  徐文涛. 青藤碱缓解氧化应激和炎症反应对四氯化碳诱导的急性肝损伤小鼠的保护作用[J]. 中国免疫学杂志, 2019, 35(8): 939-943
作者姓名:郭 华  裴高油  李龙腾  徐文涛
作者单位:郑州铁路职业技术学院药学院;郑州大学第二附属医院
基金项目:河南省科技攻关项目(082102210075)
摘    要:目的:本研究旨在探索青藤碱对四氯化碳诱导的急性肝损伤小鼠的影响。方法:小鼠随机分为4组:健康对照组(Ctrl),青藤碱组(Sinomenine),CCl_4模型组(CCl_4),青藤碱处理组(CCl_4+Sinomenine)。利用四氯化碳诱导的急性肝损伤小鼠模型。酶联免疫吸附实验(ELISA)检测天门冬氨酸氨基转移酶(AST)、丙氨酸转氨酶(ALT)、超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)、白细胞介素(IL-6)、IL-1β和肿瘤坏死因子(TNF-α)水平。苏木素伊红(HE)染色观察肝脏组织病变。脱氧核糖核苷酸末端转移酶介导的缺口末端标记(TUNEL)染色检测肝脏组织细胞凋亡。蛋白印迹检测Bcl-2和Bax表达。结果:CCl_4模型组ALT和AST水平高于对照组(P<0. 01)。与CCl_4模型组相比,青藤碱处理组ALT和AST水平下降(P<0. 01)。青藤碱可缓解四氯化碳诱导的急性肝损伤小鼠肝脏组织病变。CCl_4模型组细胞凋亡高于对照组(P<0. 01)。青藤碱处理组细胞凋亡低于CCl_4模型组(P<0. 01)。与对照组相比,CCl_4模型组Bcl-2表达减弱,Bax表达增强(P<0. 01)。与CCl_4模型组相比,青藤碱处理组Bcl-2表达上升,Bax表达下降(P<0. 01)。与对照组相比,CCl_4模型组SOD和GSH水平降低,MDA水平升高(P<0. 01)。与CCl_4模型组相比,青藤碱处理组SOD和GSH水平上升,MDA水平下降(P<0. 01)。CCl_4模型组IL-6,IL-1β和TNF-α水平高于对照组(P<0. 01)。青藤碱处理组IL-6、IL-1β和TNF-α水平低于CCl_4模型组(P<0. 01)。结论:青藤碱可减轻四氯化碳诱导的急性肝损伤小鼠肝损伤、细胞凋亡、氧化应激及炎症反应。

关 键 词:青藤碱  肝损伤  凋亡  氧化应激  炎症反应

Protective effects of sinomenine on carbon tetrachloride-induced acute hepatic injury mice by relieving oxidative stress and inflammatory reaction
GUO Hua,PEI Gao-You,LI Long-Teng,XU Wen-Tao. Protective effects of sinomenine on carbon tetrachloride-induced acute hepatic injury mice by relieving oxidative stress and inflammatory reaction[J]. Chinese Journal of Immunology, 2019, 35(8): 939-943
Authors:GUO Hua  PEI Gao-You  LI Long-Teng  XU Wen-Tao
Affiliation:(College of Pharmacy,Zhengzhou Railway Vocational and Technical College,Zhengzhou 451460,China)
Abstract:Objective:The study aims to explore the effects of sinomenine on carbon tetrachloride-induced acute hepatic injury mice.Methods:Mice were randomly divided into four groups:healthy control group(Ctrl),sinomenine group,CCl4 model group(CCl4)and sinomenine treatment group(CCl4^+Sinomenine).The model of acute hepatic injury was induced by CCl 4.The levels of aspartate aminotransferase(AST),alanine aminotransferase(ALT),superoxide dismutase(SOD),methane dicarboxylic aldehyde(MDA),glutathione(GSH),interleukin(IL)-6,IL-1βand tumor necrosis factor alpha(TNF-α)were tested by enzyme-linked immunosorbent assay(ELISA).The pathological changes of liver tissues were observed by hematoxylin-eosin(HE)staining.Apoptosis of liver tissues was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick labeling(TUNEL)staining.The expression of Bcl-2 and Bax was measured by Western blot.Results:The levels of ALT and AST in CCl 4 group were higher than control group(P<0.01).Compared with CCl 4 group,the levels of ALT and AST in CCl 4^+Sinom group were reduced(P<0.01).The pathological changes of liver tissues in CCl 4-induced acute hepatic injury mice were relieved by sinomenine.The apoptosis in CCl 4 group was higher than control group(P<0.01).The apoptosis in CCl 4+Sinom group was lower than CCl 4 group(P<0.01).Compared with control group,the expression of Bcl-2 in CCl 4 group was attenuated with enhacive expression of Bax(P<0.01).Compared with CCl 4 group,the expression of Bcl-2 in CCl 4+Sinom group was eleveated with declined expression of Bax(P<0.01).Compared with control group,the levels of SOD and GSH in CCl 4 group were decreased with enhanced levels of MDA(P<0.01).Compared with CCl 4 group,the levels of SOD and GSH in CCl 4+Sinom group were increased with reduced levels of MDA(P<0.01).The levels of IL-6,IL-1βand TNF-αin CCl 4 group were higher than control group(P<0.01).The levels of IL-6,IL-1βand TNF-αin CCl 4+Sinom group were lower than CCl 4 group(P<0.01).Conclusion:Sinomenine alleviates the liver injury,apoptosis,oxidative stress and inflammatory response in CCl 4-induced acute hepatic injury mice.
Keywords:Sinomenine  Liver injury  Apoptosis  Oxidative stress  Inflammatory response
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