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目的研究大鼠急性一氧化碳中毒(ACOP)后脑中白细胞介素-1β(IL-1β)、γ-干扰素(γ- IFN)表达的特点。方法体重240-280 g雄性SD大鼠,经预实验确定染毒剂量,于动物实验高压氧舱内行急性一氧化碳(CO)暴露,于染毒后3,7,10,20 d取脑组织,常规制备石蜡病理切片,行HE染色及 IL-1β,γ-IFN免疫组化染色,观察ACOP后大鼠脑皮质及海马神经元的病理性改变及脑中IL-1β,γ-IFN 表达的情况。结果病理学检查发现,与对照组相比,CO暴露组大鼠染毒后3-20 d脑中皮质及海马有明显的神经元变性坏死,以7和10 d最为明显,免疫组化染色发现HE染色显示的神经元变形坏死区域有大量神经元细胞和胶质细胞表达IL-1β,γ-IFN。结论 ACOP后大鼠脑中出现IL-1β,γ-IFN的迟发性表达,CD4+T淋巴细胞介导的免疫炎症反应可能参与了ACOP后迟发性神经元损伤的过程。
Objective To investigate the expression of interleukin-1β (IL-1β) and γ-interferon (γ-IFN) in the brain following acute carbon monoxide poisoning (ACOP) in rats. Methods Male Sprague-Dawley rats weighing 240-280 g were pretreated with exposure dose of Acute Exposure to Carbon Monoxide (CO) in vivo. Animals were sacrificed at 3, 7, 10, and 20 d after exposure. Conventional Paraffin sections were prepared and stained with hematoxylin-eosin (HE), IL-1β and γ-IFN by immunohistochemistry. Pathological changes of cerebral cortex and hippocampal neurons were observed after ACOP and the expression of IL-1β and γ-IFN in brain were observed. Results Compared with the control group, the neuronal degeneration and necrosis in cerebral cortex and hippocampus were found in 3-20 days after exposure in CO-exposed group, and the most obvious was at 7 and 10 days in the CO-exposed group. The results of immunohistochemistry HE staining showed a large number of neurons and glial cells express IL-1β, γ-IFN in the area of neuronal degeneration and necrosis. Conclusions The delayed expression of IL-1β and γ-IFN in rat brain after ACOP and the inflammatory and inflammatory responses mediated by CD4 + T lymphocytes may be involved in the process of delayed neuronal injury after ACOP.