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首页> 外文期刊>Experimental and therapeutic medicine >Chinese medicinal formula, Qinggan Huoxue Recipe protects rats from alcoholic liver disease via the lipopolysaccharide-Kupffer cell signal conduction pathway
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Chinese medicinal formula, Qinggan Huoxue Recipe protects rats from alcoholic liver disease via the lipopolysaccharide-Kupffer cell signal conduction pathway

机译:中药清肝活血方通过脂多糖-枯否细胞信号传导途径保护大鼠免于酒精性肝病

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摘要

The Chinese medicinal formula, Qinggan (QG) Huoxue (HX) Recipe (R) exerts a range of pharmacological effects, including reversible steatosis, decreased levels of inflammatory cytokines and lipid peroxidation resistance. The aim of the present study was to determine the specific mechanisms of QGHXR hepatoprotection through the lipopolysaccharide-Kupffer cell (LPS-KC) signal conduction pathway in rats with alcoholic liver disease (ALD). ALD rats were exposed to the compound factors, QGR and HXR. Hematoxylin and eosin staining was conducted to evaluate the pathological changes in the liver following QGHXR treatment and an enzyme-linked immunosorbent assay was performed to measure the content of tumor necrosis factor (TNF)-α in the plasma. Immunohistochemical staining was conducted to examine the expression of cell differentiation antigen (CD) 68 and 14. In addition, western blot analysis and reverse transcription-polymerase chain reaction were used to measure the expression of Toll-like receptor 4 (TLR4), phosphorylated-extracellular regulated protein kinases (p-ERK), nuclear factor (NF)-κB, CD14 and TNF-α. Following stimulation with the compound factors, the rats exhibited increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, as well as marked pathological changes. Furthermore, the related molecules in the LPS-KC pathway were upregulated and QGHXR was identified to be effective in the LPS-KC signal conduction pathway in the ALD rats. QGHXR was superior to QGR and HXR in reducing the serum ALT and AST levels, regulating CD14, TLR4, NF-κB, ERK and TNF-α as well as improving the pathological changes. The results indicated that QGHXR therapy may provide a novel strategy for treating ALD via regulation of the related molecules in the LPS-KC signaling pathway.
机译:中药配方清肝活血方药具有多种药理作用,包括可逆性脂肪变性,炎性细胞因子水平降低和脂质过氧化抗性。本研究的目的是通过酒精性肝病(ALD)大鼠中的脂多糖-库普弗细胞(LPS-KC)信号传导途径确定QGHXR保肝的具体机制。 ALD大鼠暴露于复合因子QGR和HXR。进行苏木精和曙红染色以评估QGHXR治疗后肝脏的病理变化,并进行酶联免疫吸附测定以测量血浆中肿瘤坏死因子(TNF)-α的含量。进行了免疫组织化学染色以检测细胞分化抗原(CD)68和14的表达。此外,使用Western印迹分析和逆转录聚合酶链反应来测量Toll样受体4(TLR4),磷酸化的TLR的表达。细胞外调节蛋白激酶(p-ERK),核因子(NF)-κB,CD14和TNF-α。在用复合因子刺激后,大鼠表现出增加的丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)水平,以及明显的病理变化。此外,LPS-KC途径中的相关分子被上调,并且QGHXR被确认对ALD大鼠的LPS-KC信号传导途径有效。 QGHXR在降低血清ALT和AST水平,调节CD14,TLR4,NF-κB,ERK和TNF-α以及改善病理变化方面优于QGR和HXR。结果表明,QGHXR疗法可能通过调节LPS-KC信号通路中的相关分子,为ALD治疗提供新的策略。

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