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本文研究γ 干扰素受体免疫球蛋白融合蛋白 (IFN γR Ig )对ConA诱导的小鼠细胞免疫性肝损伤的保护作用及机制。在Balb/c小鼠体内一次性静脉注射ConA 2 0mg/kg诱导细胞免疫性肝损伤模型 ,分别于模型建立前后不同时间腹腔注射 10mg/kgIFN γR Ig,观察该融合蛋白对小鼠血清谷丙转氨酶 (GPT )水平 ,细胞因子IFN γ、TNF α和IL 10分泌以及肝组织病理学变化的影响。结果表明IFN γR Ig预防给药明显改善肝脏损伤的组织学和血清学变化 ,降低GPT水平 ,减少肝脏中性粒细胞、单核细胞浸润 ;同时与模型对照小鼠相比血清IFN γ水平下降 ,TNF α分泌合成减少 ,IL 10水平明显增加。而IFN γR Ig通过早期结合并阻断内源性IFN γ ,提高IL 10的抗炎作用 ,减轻炎症细胞对肝脏的侵袭及IFN γ、TNF α的肝细胞破坏作用 ,保护免疫性肝损伤。
This study was to investigate the protective effect and mechanism of interferon gamma receptor immunoglobulin fusion protein (IFN-γR Ig) on ConA-induced cellular immunity in mice. A single intravenous injection of ConA 2 0mg / kg into Balb / c mice induced cellular immunity of liver injury models, respectively, before and after the model was established by intraperitoneal injection of 10mg / kg IFNγRg Ig, observe the fusion protein on mouse serum alanine aminotransferase (GPT), the secretion of cytokines IFNγ, TNFα and IL-10 and the pathological changes of liver tissue. The results showed that IFNγR Ig administration significantly improved histological and serological changes of liver injury, decreased GPT levels and decreased hepatic neutrophil and monocyte infiltration; at the same time compared with the model control mice serum IFN γ levels decreased, TNFα secretion decreased synthesis, IL 10 levels increased significantly. IFNγR Ig can enhance the anti-inflammatory effects of IL-10 and reduce the invasion of inflammatory cells to liver and the destruction of hepatocytes induced by IFNγ and TNFα through early binding and blocking of endogenous IFNγ, so as to protect immune liver injury.