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作 者:周琴 马莉 蒋序杰 万敬员[2] 王彬[1] Zhou Qin;Ma Li;Jiang Xujie;Wan Jingyuan;Wang Bin(Department of Anesthesiology,First Affiliated Hospital of Chongqing Medical University,Chongqing,400016;College of Pharmacy,Chongqing Medical University,Chongqing,400016)
机构地区:[1]重庆医科大学附属第一医院麻醉科,重庆400016 [2]重庆医科大学药学院,重庆400016
出 处:《基因组学与应用生物学》2020年第4期1852-1858,共7页Genomics and Applied Biology
基 金:国家自然科学基金(No.81373870);卫生部国家临床重点专科建设项目[财社(2011)170号];重庆市医学重点学科(渝卫科教(No 2007)2号)共同资助。
摘 要:探讨阿魏酸(ferulic acid,FA)对刀豆蛋白A(concanavalin A,Con A)诱导的免疫性肝损伤是否有保护作用。将雄性Balb/c小鼠随机分成6组:空白组、阿魏酸对照组(100 mg/kg)、模型组(15 mg/kg Con A)、低剂量阿魏酸干预组(10 mg/kg)、中剂量阿魏酸干预组(30 mg/kg)、高剂量阿魏酸干预组(100 mg/kg)。阿魏酸灌胃后,尾静脉注射刀豆蛋白A 15 mg/kg,24 h后,取其血和肝组织进行检测。与空白组比较,模型组中苏木精和伊红染色(HE)坏死区域明显增加,丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)水平、半胱天冬氨酸酶3(Caspase-3)活性、肿瘤坏死因子-α(TNF-α)和干扰素-γ(IFN-γ)水平、CD4^+T细胞中CD69的表达都明显增高。与模型组相比,阿魏酸干预组的ALT和AST水平明显降低,呈剂量依赖性,HE坏死区域减少,Caspase-3活性、TNF-α和IFN-γ水平、CD4^+T细胞CD69的表达都明显降低,且具有统计学意义。表明阿魏酸对刀豆蛋白A诱导的免疫性肝损伤有保护作用,其机制可能是抑制CD4^+T淋巴细胞的活化、细胞因子的释放,减轻炎症和肝组织的凋亡。To investigate whether Ferulic acid(FA)has a protective effect on immune liver injury induced by Concanavalin A(Con A).Male Balb/c mice were randomly divided into 6 groups:Blank group,ferulic acid control group(100 mg/kg,po),model group(15 mg/kg Con A,iv),low dose ferulic acid intervention group(10 mg/kg),medium dose ferulic acid intervention group(30 mg/kg)and high dose ferulic acid intervention group(100 mg/kg).After given ferulic acid by gavage,mice were intravenous injection of concanavalin A 15 mg/kg.After 24 h,the blood and liver tissue were taken for detection.Compared with the blank group,hematoxylin and eosin(HE)necrosis area were increased,ALT and AST levels,Caspase-3 activity,IFN-γ,TNF-αlevels and CD69 expression of CD4^+T cells were significantly higher in model group.Compared with model group,ALT and AST levels were significantly decreased in dose-dependent manner,HE necrosis area,Caspase-3 activity,IFN-γ,TNF-αlevels and CD69 expression of CD4^+T cells were significantly decreased in ferulic acid intervention group.Ferulic acid has a protective effect on Concanavalin A induced immunity liver injury.Its mechanism may be to inhibit the activation of CD4^+T lymphocytes,the release of cytokines,reduce the inflammation and the apoptosis of liver tissues.
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