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目的 :观察 IFN- γ激活的巨噬细胞 ( MΦ)合成的一氧化氮 ( NO)及其在疟疾保护性免疫中杀伤疟原虫的作用。方法 :体外分离培养小鼠腹腔 MΦ,与不同浓度的 γ干扰素 ( IFN- γ)共育 4 8h后 ,加入分离的寄生疟原虫的红细胞 ,观察激活的 MΦ NO产生水平及其对疟原虫的杀伤作用。结果 :IFN-γ能激活 MΦ产生 NO,其产生的量与 IFN-γ的浓度有关 ;MΦ对疟原虫的杀伤作用与 NO的释放量呈显著相关关系 ( r=0 .898,n=13,P<0 .0 1) ;N-硝基 - L -精氨酸 ( N- nitro-L- arginine,L- NNA)能抑制 NO合成 ,同时也降低 MΦ 的杀伤活性 ;感染约氏疟原虫的 BAL B/c小鼠注射 L- NNA,导致原虫血症上升 ,小鼠死亡率升高。结论 :IFN- γ激活 MΦ产生 NO可能是杀伤疟原虫的重要作用机制。
Objective: To observe the synthesis of nitric oxide (NO) by IFN-γ-activated macrophages (MΦ) and its role in killing malaria parasite in protective immunity against malaria. Methods: The peritoneal MΦ was isolated and cultured in vitro for 48 hours with different concentrations of interferon-γ (IFN-γ), and the isolated erythrocytes of parasitic malariae were added to observe the level of activated MΦ-NO and its effect on Plasmodium Killing effect. Results: The production of NO by MΦ was activated by IFN-γ, and its production was related to the concentration of IFN-γ. The killing effect of MΦ on Plasmodium had a significant correlation with the release of NO (r = 0.988, n = 13, P <0.01). N-nitro-L-arginine (N-nitro-L-arginine) inhibited the synthesis of NO and reduced the activity of MΦ. Plasmodium yoelii Injection of L-NNA into BAL B / c mice led to an increase in parasitemia and increased mortality in mice. Conclusion: IFN-γ-activated MΦ produce NO may be an important mechanism of killing Plasmodium.