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首页> 外文期刊>Cell biochemistry and biophysics >Neuroprotective Effect of Atorvastatin Involves Suppression of TNF-α and Upregulation of IL-10 in a Rat Model of Intracerebral Hemorrhage
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Neuroprotective Effect of Atorvastatin Involves Suppression of TNF-α and Upregulation of IL-10 in a Rat Model of Intracerebral Hemorrhage

机译:阿托伐他汀的神经保护作用涉及脑出血大鼠模型中TNF-α的抑制和IL-10的上调。

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摘要

We evaluated the neuroprotective effects of atorvastatin (2, 5, and 10 mg/kg) on experimentally induced intracerebral hemorrhage (ICH) in adult rats; controls were administered PBS. Plasma TNF-α and IL-10 levels before and after ICH were analyzed at various time points by enzyme-linked immunosorbent assay (ELISA) and neurological behavior of rats was assessed by climbing scores. At 3-days postoperatively, brain water contents and TNF-α/IL-10 expression in brain tissue were determined. Histopathological changes and microglial cells in the brain tissue were evaluated by light-microscopy. Post-ICH neurological deficits differed significantly between sham-operated group A and experimental-ICH group B (P < 0.05). Brain water contents were significantly less in group A than in group B (P < 0.05). Significant differences (P < 0.05) between two groups were observed regarding activated microglia, TNF-α and IL-10 levels. Compared with group B, neurological deficits, brain water contents, pathological changes, and activated microglia were reduced (P < 0.05) in groups C (Experimental-ICH + atorvastatin 2 mg/kg), D (Experimental-ICH + atorvastatin 5 mg/kg) and E (Experimental-ICH + atorvastatin 10 mg/kg). Atorvastatin-induced a dose-dependent reduction of TNF-α and increase of IL-10 levels (P < 0.05). Therefore, it was concluded that atorvastatin improved neurofunctional rehabilitation in rats through the suppression of cytokines-mediated inflammatory response and attenuation of brain damage following intracerebral hemorrhage.
机译:我们评估了阿托伐他汀(2、5和10 mg / kg)对成年大鼠实验性脑出血(ICH)的神经保护作用。对照被给予PBS。通过酶联免疫吸附试验(ELISA)在不同时间点分析ICH前后血浆TNF-α和IL-10的水平,并通过攀登评分评估大鼠的神经行为。术后3天,测定脑组织中脑水含量和TNF-α/ IL-10表达。通过光学显微镜评估脑组织中的组织病理学变化和小胶质细胞。假手术组A和实验性ICH组之间ICH后神经功能缺损有显着差异(P <0.05)。 A组的脑含水量明显少于B组(P <0.05)。在活化的小胶质细胞,TNF-α和IL-10水平上,两组之间存在显着差异(P <0.05)。与B组相比,C组(实验性ICH +阿托伐他汀2 mg / kg),D组(实验性ICH +阿托伐他汀5 mg / kg)减少了神经功能缺损,脑水含量,病理变化和活化的小胶质细胞(P <0.05)。公斤)和E(实验性ICH +阿托伐他汀10毫克/公斤)。阿托伐他汀诱导TNF-α剂量依赖性降低和IL-10水平升高(P <0.05)。因此,可以得出结论,阿托伐他汀通过抑制细胞因子介导的炎症反应和减轻脑出血后脑损伤的改善来改善大鼠的神经功能康复。

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