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目的:探讨波棱瓜子有效成分波棱素抗Con A诱导的免疫性肝损伤作用机制。方法:一次性给予动物尾静脉注射刀豆求(球)蛋白(20mg/kg)造成小鼠免疫性肝损伤模型,取肝脏组织,考察药物对诱导型一氧化氮合酶(iNOS)、白细胞介素-4(IL-4)、肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)、细胞因子信号传导抑制蛋白1(SOCS1)和核因子-κB(NF-κB)的影响。结果:HE显示肝细胞出现肿胀与坏死,部分出现细胞变形,说明Con A诱导肝损伤模型造模成功。波棱素给药后发现,与模型组对比,20mg/kg剂量组NF-κB、TNF-α、IFN-γ、iNOS和IL-4酶活性有不同程度的下降;HE显示各组肝细胞不同程度的损伤,部分肝细胞坏死,与模型组比较波棱素各组细胞破坏程度较轻,肝窦之间的炎症因子变少。结论:波棱素可降低Con A引起的肝损伤的酶活力,保护肝脏组织免受侵害,其机制可能与提高自身的抗氧化能力和抑制TNF-α/NF-κB信号通路,减少炎症反应有关。
OBJECTIVE: To investigate the mechanism of action of rifampicin against Con A on immune liver injury induced by melphalan. Methods: The mouse model of autoimmune liver injury was induced by a single injection of sodium dodecylbenzenesulfonate (20 mg / kg) into the tail vein of mice and the liver tissue was taken. The effects of drugs on iNOS, IL-4, TNF-α, IFN-γ, SOCS1 and NF-κB, Impact. Results: Hematoxylin and eosin (HE) showed swelling and necrosis of hepatocytes, and cell degeneration in some cases, indicating that Con A induced liver injury model was successfully established. Compared with the model group, the activity of NF-κB, TNF-α, IFN-γ, iNOS and IL-4 in the 20 mg / Degree of injury, some of the liver cells necrosis, compared with the model group, the degree of cell damage in each group of mitomycin lighter, sinusoidal sinusitis less inflammatory factors. CONCLUSION: Glycyrrhizin can reduce the enzyme activity of liver injury caused by Con A and protect the liver from infiltration. The mechanism may be related to improving its antioxidant capacity and inhibiting TNF-α / NF-κB signaling pathway and reducing the inflammatory reaction .