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首页> 美国卫生研究院文献>Journal of the Boston Society of Medical Sciences >Dexamethasone inhibits induction of liver tumor necrosis factor-alpha mRNA and liver growth induced by lead nitrate and ethylene dibromide.
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Dexamethasone inhibits induction of liver tumor necrosis factor-alpha mRNA and liver growth induced by lead nitrate and ethylene dibromide.

机译：地塞米松抑制由硝酸铅和二溴乙烷引起的肝肿瘤坏死因子-αmRNA的诱导和肝生长。

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We have recently demonstrated that a single injection of the mitogen lead nitrate to rats induced a rapid increase of tumor necrosis factor-alpha (TNF-alpha) mRNA in the liver and suggested that this cytokine may be involved in triggering hepatocyte proliferation in this model of direct hyperplasia. In this study, we examined whether a similar induction of liver TNF-alpha mRNA could be observed preceding the onset of hepatocyte proliferation induced by ethylene dibromide, another hepatocyte mitogen. In addition, we used dexamethasone, a well known inhibitor of TNF-alpha production, to determine whether its administration could suppress hepatocyte proliferation induced by lead nitrate and ethylene dibromide. A single intragastric administration of ethylene dibromide (100 mg/kg) to male Wistar rats enhanced liver TNF-alpha mRNA after 4 and 7 hours, which then returned to control levels by 24 hours. TNF-alpha mRNA was detectable only in a nonparenchymal cell fraction of the liver. Pretreatment of rats with a single dose of dexamethasone (2 mg/kg) 60 minutes before lead nitrate (100 mumol/kg) or ethylene dibromide completely abolished the increased levels of liver TNF-alpha mRNA induced by these agents. Inhibition by dexamethasone of TNF-alpha mRNA was associated with an inhibition of liver cell proliferation induced by these mitogens, as measured by [3H]thymidine incorporation into hepatic DNA, mitotic index, and DNA content. These results further support the hypothesis that TNF-alpha may be involved in triggering hepatocyte proliferation induced by primary mitogens.
机译：我们最近证明，向大鼠单次注射丝裂原硝酸铅会诱导肝脏中肿瘤坏死因子-α（TNF-α）mRNA的快速增加，并表明该细胞因子可能参与了该模型的肝细胞增殖。直接增生。在这项研究中，我们检查了在另一种肝细胞有丝分裂原亚乙基二溴化物诱导的肝细胞增殖开始之前，是否可以观察到类似的肝TNF-αmRNA诱导。另外，我们使用了地塞米松（一种众所周知的TNF-α抑制剂）来确定其给药是否可以抑制硝酸铅和二溴乙烷导致的肝细胞增殖。对雄性Wistar大鼠单次胃内给予二溴乙烷（100 mg / kg），可在4和7小时后增强肝脏TNF-αmRNA，然后在24小时后恢复至对照水平。 TNF-αmRNA仅在肝脏的非实质细胞部分中可检测到。在硝酸铅（100μmol/ kg）或二溴化乙锭完全消灭之前，用单剂量地塞米松（2 mg / kg）预处理大鼠完全消除了由这些试剂诱导的肝脏TNF-αmRNA水平升高。地塞米松对TNF-αmRNA的抑制作用与抑制这些有丝分裂原诱导的肝细胞增殖有关，如通过将[3H]胸苷掺入肝DNA，有丝分裂指数和DNA含量所测量的。这些结果进一步支持了以下假设：TNF-α可能参与触发由原代有丝分裂原诱导的肝细胞增殖。

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