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首页> 外文期刊>Journal of Cellular Physiology >Uncoupling protein-2 induction in rat hepatocytes after acute carbon tetrachloride liver injury.
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Uncoupling protein-2 induction in rat hepatocytes after acute carbon tetrachloride liver injury.

机译：解偶联protein-2诱导大鼠肝细胞后急性四氯化碳肝损伤。

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摘要

This study is focused on the role of UCP-2 in hepatic oxidative metabolism following acute CCl(4) administration to rats. UCP-2 mRNA, almost undetectable in the liver of controls, was significantly increased 24 h after CCl(4) administration, peaked at 72 h and then tended to disappear. UCP-2 protein, undetectable in controls, increased 48-72 h after CCl(4) treatment. Experiments with isolated liver cells indicated that in control rats UCP-2 was expressed in non-parenchymal cells and not in hepatocytes, whereas in CCl(4)-treated rats UCP-2 expression was induced in hepatocytes and was not affected in non-parenchymal cells. Addition of CCl(4) to the culture medium of hepatocytes from control rats failed to induce UCP-2 expression. Liver mitochondria from CCl(4)-treated rats showed an increase of H(2)O(2) release at 12-24 h, followed by a rise of TBARS. Vitamin E protected liver from CCl(4) injury and reduced the expression of UCP-2. Treatment with GdCl(3) prior to CCl(4), in order to inhibit Kupffer cells, reduced TBARS and UCP-2 mRNA increase in hepatic mitochondria. Our data indicate that CCl(4) induces the expression of UCP-2 in hepatocytes with a redox-dependent mechanism involving Kupffer cells. A role of UCP-2 in moderating CCl(4)-induced oxidative stress during tissue regeneration after injury is suggested.
机译：本研究关注UCP-2的作用急性后肝氧化代谢创新领导力的老鼠(4)政府。察觉在肝脏的控制CCl显著增加后24 h (4)管理,达到峰值72 h,然后往往消失。CCl控制,增加后48 - 72 h (4)治疗。表明在控制老鼠UCP-2而不是在表达non-parenchymal细胞肝细胞,而在CCl(4)治疗大鼠UCP-2分部表达诱导肝细胞和不是在non-parenchymal细胞的影响。CCl(4)肝细胞的培养基控制老鼠未能诱导UCP-2表达式。从CCl(4)治疗大鼠肝线粒体显示增加H (2) O(2)释放在12 - 24h,增加TBARS紧随其后。CCl保护肝脏免受(4)损伤和减少UCP-2的表达。CCl(4)之前,为了抑制枯氏细胞,减少TBARS和UCP-2 mRNA的增加肝线粒体。CCl(4)诱发UCP-2的表达肝细胞redox-dependent机制涉及枯氏细胞。全身的CCl缓和(4)氧化应激组织再生后受伤。

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