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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >IL-1 or TNF receptor gene deletion delays onset of encephalopathy and attenuates brain edema in experimental acute liver failure.
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IL-1 or TNF receptor gene deletion delays onset of encephalopathy and attenuates brain edema in experimental acute liver failure.

机译：在实验性急性肝衰竭中，IL-1或TNF受体基因的缺失会延迟脑病的发作并减轻脑水肿。

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Previous reports suggested that brain-derived proinflammatory cytokines are involved in the pathogenesis of hepatic encephalopathy (HE) and brain edema in acute liver failure (ALF). To further address this issue, expression of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) mRNAs were measured in the brains of mice with acute liver failure resulting from exposure to azoxymethane. In addition, time to severe encephalopathy (coma) was assessed in mice lacking genes coding for interferon-gamma, the tumor necrosis factor receptor-1 or the interleukin-1 type 1 receptor. Interleukin-1beta, tumor necrosis factor-alpha and interferon-gamma expression were quantified using RT-PCR. Significant increases in interleukin-1beta and tumor necrosis factor-alpha mRNA were observed in the frontal cortex of azoxymethane-treated wild-type mice at coma stages of encephalopathy. Interferon-gamma, however, could not be detected in the brains of these animals. Onset of severe encephalopathy (coma) and brain edema in ALF mice were significantly delayed in interleukin-1 type 1 receptor or tumor necrosis factor receptor-1 knockout mice. Deletion of the interferon-gamma gene, on the other hand, had no significative effect on the neurological status or brain water content of acute liver failure mice. These results demonstrate that toxic liver injury resulting from exposure to azoxymethane is associated with selective induction of proinflammatory cytokines in the brain and that deletion of tumor necrosis factor receptor-1 or interlukin-1 type 1 receptor delays the onset of coma and brain edema in this model of acute liver failure. These findings further support a role for selective brain-derived cytokines in the pathogenesis of the cerebral complications in acute liver failure and suggest that anti-inflammatory strategies could be beneficial in their prevention.
机译：先前的报道表明，脑源性促炎细胞因子参与急性肝衰竭（ALF）的肝性脑病（HE）和脑水肿的发病机理。为了进一步解决这个问题，在由以下原因导致的急性肝衰竭小鼠的大脑中测量了白介素-1β（IL-1beta），肿瘤坏死因子-α（TNF-alpha）和干扰素-γ（IFN-γ）mRNA的表达。暴露于乙氧基甲烷。另外，在缺乏编码干扰素-γ，肿瘤坏死因子受体-1或白介素-1型受体基因的小鼠中评估了严重脑病（昏迷）的时间。使用RT-PCR定量测定白细胞介素1β，肿瘤坏死因子-α和干扰素-γ的表达。在脑病昏迷期，用乙氧甲烷处理的野生型小鼠的额叶皮层中观察到白介素-1β和肿瘤坏死因子-αmRNA的显着增加。但是，在这些动物的大脑中无法检测到γ-干扰素。白细胞介素1 1型受体或肿瘤坏死因子受体1基因敲除小鼠在ALF小鼠中严重脑病（昏迷）和脑水肿的发作明显延迟。另一方面，干扰素-γ基因的删除对急性肝衰竭小鼠的神经系统状态或脑含水量没有显着影响。这些结果表明，暴露于乙氧基甲烷导致的中毒性肝损伤与脑中促炎性细胞因子的选择性诱导有关，并且肿瘤坏死因子受体1或白细胞介素1型1受体的缺失延迟了昏迷和脑水肿的发作。急性肝衰竭模型。这些发现进一步支持选择性脑源性细胞因子在急性肝衰竭的脑并发症的发病机制中的作用，并表明抗炎策略可能对其预防有益。

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