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主要组织相容性复合体Ⅱ和γ-干扰素在CO中毒迟发性脑病大鼠模型脑内的表达 被引量:3

Expression of MHC Ⅱ and IFN-γ in rat models of delayed neuropathological sequelae after CO poisoning
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摘要 目的探讨CO中毒迟发性脑病(DNS)大鼠模型脑内主要组织相容性复合体Ⅱ(MHCⅡ)和γ-干扰素(IFN-γ)的表达,分析其发病机制。方法建立CO中毒DNS大鼠模型,用HE染色观察大鼠脑组织病理学变化,用免疫组织化学方法检测大鼠脑内MHCⅡ和IFN-γ的表达。结果HE染色标本上,正常对照组大鼠脑内细胞形态正常,DNS大鼠脑皮质出现大片疏松区,海马锥体细胞层稀疏,可见点片状坏死。免疫组化结果显示,对照组无或仅有少量MHCⅡ和IFN-γ表达;DNS组有表达,MHCⅡ3d表达增强,7d达高峰,10d呈零星分布,20d几乎无阳性细胞;IFN-γ3d表达高峰,7d有所下降, 10d、20d呈零星分布。结论与对照组相比,DNS大鼠脑组织存在明显的病理学改变,MHCⅡ和IFN-γ的表达明显增多,且在时间上有一定顺序,提示免疫因素可能参与了DNS的发病过程。 Objective To study the expression of MHC Ⅱ and IFN-γ in rat models of delayed neuropathological sequelae (DNS) after CO poisoning, and to analyse the mechanism of DNS. Methods Establishing models of DNS, HE staining was used to observe the pathological changes of brain tissues and immunohistochemical staining was used to observe the expression of MHC Ⅱ and IFN-γ. Results HE staining showed that the morphology of neurons in the normal control (NC) group was normal ; the cortex of the DNS groups were loose, and the cone cells of hippecampus were thin and necrotic. Immunohistochemical staining showed that there was little expression of MHC Ⅱ and IFN-γ in the NC group, but in the DNS groups the expression of the two proteins was obvious. The expression of MHC Ⅱ increased on the 3rd day, peaked on the 7th day, decreased on the 10th day and disappeared on the 20th day. The expression of IFN-γpeaked on the 3rd day,decreased on the 7th day and disappeared on the 10th day and the 20th day. Conclusions Compared with the NC group, there were si^ificant pathological changes in the brains of DNS groups. The distinct expression of MHC Ⅱ and IFN-γ and the expression fastigium suggest that the pathogenic process of DNS is immune-mediated.
出处 《中华航海医学与高气压医学杂志》 CAS CSCD 2007年第1期15-18,共4页 Chinese Journal of Nautical Medicine and Hyperbaric Medicine
基金 全军“十一五”医药卫生课题(06MA213)
关键词 CO中毒 迟发性脑病 主要组织相容性复合体Ⅱ Γ-干扰素 CO poisoning Delayed neuropathological sequelae MHC Ⅱ IFN-γ
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  • 1Piantadosi CA. Carbon morioxide poisoning. Undersea Hyperb Med,, 2004, 31: 167-177.
  • 2Stephen R, Thom, Veena M, et al. Delayed neuropathology after carbon monoxide poisoning is immune-mediated. Proc Natl Acad Sci, 2004, 101: 13660-13665.
  • 3Scheinkestel CD, Bailey M, Myles PS, et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randormized controlled clinical trail. Med J, 1999, 170: 203-210.
  • 4Brown SD,piantadosi CA. Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. J Clin Invest,1992,89:666-672.
  • 5Piantadosi CA,Zhang J, Demchenco IT. Production of hydroxl radical in the hippocampus after CO hypoxia or hypoxic hypoxia in the rat.Free Radical Biol Med, 1997,22:725-732.
  • 6Piantadosi CA, Zhang J, Levin ED, et al. Apoptosis and delayed neuronal damage after carbon monoxide poisoning in the rat. Exp Neural ,2000,147 : 130-140.
  • 7Hana Kalistova ,Eva Havrdova ,Jana Uhrova, et al. Myelin basic protein in multiple sclerosis and other neurological disorders. J Neurol, 2003,250 : 874-875.
  • 8Besser M, Wank R. Cutting edge: clonally restricted production of the neurotrophins brain-derived neurotrophic factor and neurotrophin-3mRNA by human immune cells and Th1/Th2-polarized expression of their receptors. J Immunol, 1999,162:6303.
  • 9Kerschensteiner M, Gallmeier E, Behrens L, et al. Activated human T cells, B cells and monocytes produce brain-derived neurotrophic factor in vitro an d in inflammatory brain lesions:a neuroprotective role of inflammation. J Exp Med, 1999,189:865.
  • 10Kazuhiro I, Nozomi H, Makoto S, et al. Distribution of major histocompatibility complex class Ⅱ-positive microglisand cytokine profile of Parkinson's disease brains. Acta Neuropathol, 2003,106:518-526.

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