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作 者:林霖[1] 汪纪仓[1] 王宏伟[1] 张才[1] 杨自军[1]
机构地区:[1]河南科技大学动物科技学院/河南省高等学校环境与畜产品安全重点实验室,河南洛阳471023
出 处:《畜牧与兽医》2017年第11期114-117,共4页Animal Husbandry & Veterinary Medicine
基 金:河南省教育厅基础研究项目(13B230989)
摘 要:探讨水飞蓟宾对镉致小鼠急性肝损伤的保护作用及其机制。将30只小鼠随机分成3组:正常对照组、镉组、水飞蓟宾干预组。正常对照组、镉组小鼠每日灌胃1%羧甲基纤维素钠悬混液,水飞蓟宾干预组小鼠经口给予100 mg·kg^(-1)水飞蓟宾,每日灌胃1次,连续灌胃7 d,于最后一次灌胃后1 h,正常对照组小鼠腹腔注射生理盐水0.01 mL·g^(-1),镉组及水飞蓟宾干预组小鼠一次性腹腔注射4 mg·kg^(-1)氯化镉,24 h后摘小鼠眼球取血,处死小鼠。检测血清丙氨酸转移酶(ALT)、天冬氨酸转移酶(AST)活性;制作肝组织切片,H.E染色,观察各组小鼠肝组织形态学变化;免疫组化检测肝组织HSP70蛋白表达;肝组织匀浆液检测一氧化氮(NO)含量及髓过氧化物酶(MPO)活性。结果显示,镉组小鼠血清ALT和AST活性与正常对照组比较显著升高,肝细胞出现变性、坏死,水飞蓟宾干预组小鼠血清ALT和AST活性与镉组比较显著降低,同时,肝细胞变性、坏死明显减轻;免疫组化检测结果显示,镉组小鼠肝组织热应激蛋白(HSP70)表达与正常对照组比较显著降低(P<0.05),而水飞蓟宾干预组小鼠肝细胞HSP70蛋白表达与镉组比较均极显著升高(P<0.01);与正常对照组比较,染镉组小鼠肝组织一氧化氮(NO)含量及髓过氧化物酶(MPO)活性均极显著升高(P<0.01),水飞蓟宾干预组小鼠与镉组小鼠比较,肝组织NO含量和MPO活性极显著降低(P<0.01)。结果表明,水飞蓟宾能减轻镉毒性导致的小鼠肝组织细胞急性损伤,其机制可能与水飞蓟宾降低NO含量及MPO活性,促进染镉小鼠肝组织细胞HSP70蛋白表达有关。To investigate the protective effect of silibinin on acute liver damage induced by cadmium in mice,30 mice were randomly divided into three groups,including control group,cadmium(Cd) group and silibinin protective group(Cd + silibinin).The mice of silibinin protective group were continuously administrated with silibinin at a dose of 100 mg·kg^-1·d^-1 by intragastric route for 7 d.The acute liver damage was induced by cadmium chloride(4 mg·kg^-1) on mice of Cd groups and silibinin protective group on the 24 h ahead of sacrifice.Activities of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) in sera were examined; liver histophological changes were examined by H.E; the expression of heat shock protein 70(HSP70) was demonstrated by immunohistochemical staining; myeloperoxidase(MPO) activities and nitric oxide(NO) content were examined on liver tissue.The results showed that activities of ALT and AST were increased,and liver had serious pathological damage with degeneration and necrosis in mice of Cd group,while the damage was slight remarkably on liver of mice treated with silibinin.Compared with the control group,the expression of HSP70 protein was decreased remarkably on liver in mice of Cd group,while the protein expression of HSP70 was enhanced remarkably on liver in mice treat with silibinin.NO content and MPO activity were increased in mice of Cd group,while the two indexes were decreased remarkably in mice of silibinin protective group.The results indicate that silibinin can ameliorate the liver acute injury induced by cadmium,and this mechanism might be associated with inhibiting stress and promoting the HSP70 expression.
分 类 号:R144[医药卫生—公共卫生与预防医学]
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