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动脉粥样硬化是一种自身免疫性疾病。人自身热休克蛋白60是主要的自身免疫原之一,能引起人自身免疫性反应进而促进动脉粥样硬化的发生,热休克蛋白65与人热休克蛋白60有较高的同源性,同源性为46%左右,具有相似的抗原表位,通过诱导粘膜免疫耐受产生抗炎效果将会对动脉粥样硬化产生积极的影响。热休克蛋白65鼻黏膜免疫动脉粥样硬化模型新西兰大白兔,能显著减轻主动脉粥样斑块,与PBS组存在极显著差异(P<0.01)。热休克蛋白65上31~46片段,180~188片段与霍乱毒素B亚单位的融合蛋白鼻黏膜免疫动脉粥样硬化模型新西兰大白兔,不能显著减轻主动脉粥样斑块,与PBS组不存在显著性差异(P>0.05)。结果表明HSP65鼻黏膜免疫新西兰大白兔能有效诱导兔黏膜免疫耐受,预防动脉粥样硬化;热休克蛋白65上31~46片段和180~188片段,虽然有文献报道通过诱导免疫耐受在小鼠自身免疫性疾病佐剂性关节炎中有很好的预防作用,但在动脉粥样硬化中却不能有效诱导黏膜免疫耐受而显著改善病情。
Atherosclerosis is an autoimmune disease. Human self-heat shock protein 60 is one of the major autoimmune, can cause autoimmune reaction in humans and thus promote the occurrence of atherosclerosis, heat shock protein 65 and human heat shock protein 60 have high homology, About 46% of the origin, with similar antigenic epitopes, anti-inflammatory effect by inducing mucosal immune tolerance will have a positive impact on atherosclerosis. Heat shock protein 65 nasal mucosal immune atherosclerosis model New Zealand white rabbits, can significantly reduce the aortic atherosclerotic plaque, and there was a significant difference (P <0.01). New Zealand white rabbits with nasal mucosal immunological atherosclerosis model fusion proteins 31 to 46, 31 to 46, and 180 to 188 cholera toxin B subunits on heat shock protein 65 were not significantly attenuated in atherosclerotic plaque, but not in PBS group Significant difference (P> 0.05). The results showed that HSP65 nasal mucosa immunization of New Zealand white rabbits can effectively induce mucosal immune tolerance in rabbits, prevent atherosclerosis; heat shock protein 65 31 ~ 46 and 180 ~ 188 fragments, although it has been reported in the literature by inducing immune tolerance in small There is a good preventive effect in adjuvant arthritis of autoimmune diseases in mice, but it can not effectively induce mucosal immune tolerance and significantly improve the disease in atherosclerosis.