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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 silybin on acute liver injury induced by cadmium in mice and its mechanism. Thirty mice were randomly divided into three groups: normal control group, cadmium group and silybin intervention group. In the normal control group, the mice in the group of cadmium were intragastrically given 1% sodium carboxymethylcellulose suspension and the mice in the silibinin group were given orally with 100 mg · kg -1 silibinin daily The rats in the normal control group were intraperitoneally injected with 0.01 mL · g ~ (-1) saline intraperitoneally 1 h after the last intragastric administration. The mice in the cadmium group and silybin group One intraperitoneal injection of 4 mg · kg ~ (-1) cadmium chloride, 24 h after the eyeball mice were taken for blood, the mice were sacrificed. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity were detected. Liver sections were made and stained with HE for the morphological changes of liver tissue in each group. The expression of HSP70 protein in liver tissue was detected by immunohistochemistry The content of nitric oxide (NO) and myeloperoxidase (MPO) in liver homogenate were measured. The results showed that the activity of ALT and AST in serum of cadmium group was significantly higher than that of normal control group, the degeneration and necrosis of hepatocytes were observed. The serum ALT and AST activities in serum of silybin intervention group were significantly lower than those in cadmium group, meanwhile, Hepatic cell degeneration and necrosis were significantly reduced. The results of immunohistochemistry showed that the expression of heat stress protein (HSP70) in hepatic tissue of cadmium group was significantly lower than that of the normal control group (P <0.05), while the silybin group (P <0.01). Compared with the normal control group, the contents of nitric oxide (NO) and myeloperoxidase (MPO) in hepatic tissue of cadmium-exposed mice were significantly increased (P <0.01). The content of NO and the activity of MPO in liver of Silybin intervention group were significantly lower than that of Cd group (P <0.01). The results showed that silybin could reduce the acute injury of liver cells in mice induced by cadmium toxicity. The mechanism may be related to the reduction of NO and MPO activity and the expression of HSP70 in liver tissues of Cd-infected mice.