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Effect of globin digest on the liver injury and hepatic gene expression profile in galactosamine-induced liver injury in SD rats.

机译:球蛋白消化对半乳糖胺致SD大鼠肝损伤及肝基因表达谱的影响。

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AIMS: We investigated the effect of globin digest (GD) on the liver injury and hepatic gene expression profile in galactosamine (GalN)-induced liver injury. MAIN METHODS: The effect of GD on the liver injury was examined by measuring the activities of serum transferases and hepatic antioxidant enzymes, histopathological analysis, gene expression profile, and proteins of the peroxisome proliferator-activated receptor alpha (PPARalpha) and met proto-oncogene (c-Met) in SD rats at 24 h after GalN administration. The effect of GD on the expression of PPARalpha and its target gene in AML-12 mouse hepatocytes was also examined. KEY FINDINGS: GD suppressed the elevated activities of serum transferases in GalN-induced liver injury in SD rats. The thiobarbituric acid reactive substance content in GalN-injured liver was a decreasing tendency by GD. GD suppressed the increased oxidized glutathione content, and increased the decreased protein, reduced glutathione contents, and catalase activity in GalN-injured liver. GD may improve the antioxidant defense system and protein synthesis in GalN-injured liver. GD suppressed the elevated expression of the genes related to the inflammation, and decreased the histopathological grade value of inflammatory cell infiltration in GalN-injured liver. GD increased the expression of PPARalpha protein in GalN-injured liver, and also increased the expression of PPARalpha and its target gene in AML-12 hepatocytes. The total and phosphorylated c-Met proteins in GalN-injured liver were the increasing tendencies by GD. SIGNIFICANCE: These findings indicate that GD has the hepatoprotective effect on GalN-induced liver injury in SD rats.
机译:目的:我们研究了球蛋白消化(GD)对半乳糖胺(GalN)诱导的肝损伤中肝损伤和肝基因表达谱的影响。主要方法:通过测量血清转移酶和肝抗氧化酶的活性,组织病理学分析,基因表达谱以及过氧化物酶体增殖物激活受体α(PPARalpha)和原始癌基因蛋白来检测GD对肝损伤的影响。 GalN给药后24小时,SD大鼠体内的(c-Met)。还检查了GD对AML-12小鼠肝细胞中PPARalpha及其靶基因表达的影响。主要发现:GD抑制了GalN诱导的SD大鼠肝脏损伤中血清转移酶活性的升高。 GD对GalN损伤的肝脏中的硫代巴比妥酸反应性物质含量呈下降趋势。 GD抑制了GalN损伤的肝脏中氧化型谷胱甘肽含量的增加,并增加了蛋白质的减少,谷胱甘肽含量的减少和过氧化氢酶的活性。 GD可改善GalN损伤的肝脏的抗氧化防御系统和蛋白质合成。 GD抑制了与炎症相关的基因的表达升高,并降低了GalN损伤的肝脏中炎症细胞浸润的组织病理学分级值。 GD增加了GalN损伤的肝脏中PPARalpha蛋白的表达,并且还增加了AML-12肝细胞中PPARalpha及其靶基因的表达。 GD对GalN损伤的肝脏中总的c-Met蛋白和磷酸化的c-Met蛋白呈增加趋势。意义:这些发现表明GD对GalN诱导的SD大鼠肝损伤具有保肝作用。

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