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目的:观察沙土鼠脑缺血组织学变化及肿瘤坏死因子(TNF)、白介素 1(IL 1)不同时间点的变化及大黄素甲醚对TNF和IL 1 的影响,探讨大黄素甲醚防治脑缺血性损伤的可能机制。方法:80 只雄性蒙古沙土鼠随机分为缺血组及假手术对照组,缺血组又分为大黄素甲醚治疗组及安慰剂组。分别测定各组不同时间点脑组织中TNF、IL 1的含量及观察其组织学变化。结果:缺血组中TNF、IL 1表达分别于1 小时和3 小时开始显著增加,且随缺血时间延长,其表达迅速增加;而大黄素甲醚治疗组TNF和IL 1 增加不明显,组织学中其神经组织变性、坏死及血管炎性反应也明显减轻。结论:缺血脑组织中随组织变性坏死TNF、IL 1表达增加,而大黄素甲醚可减轻缺血性病理损害,这种作用可能是通过抑制TNF、IL 1的过度表达而实现的。
Objective: To observe the histological changes of cerebral ischemia in gerbils, the changes of tumor necrosis factor (TNF) and interleukin-1 (IL 1) at different time points and the effects of emodin on TNF and IL 1 and to explore the effects of rhein methyl ether on brain protection. Possible mechanisms of ischemic injury. METHODS: Eighty male Mongolian gerbils were randomly divided into ischemic group and sham-operated control group. The ischemic group was divided into emodin-treated group and placebo group. The contents of TNF and IL 1 in brain tissue at different time points in each group were measured and their histological changes were observed. Results: The expression of TNF and IL 1 in the ischemic group began to increase significantly at 1 hour and 3 hours, respectively. The expression of TNF and IL 1 increased rapidly with the prolongation of ischemic time. However, the increase of TNF and IL 1 was not obvious in the treatment group of rhubarb. Neurological degeneration, necrosis, and vasculitis were also significantly reduced in the study. Conclusion: The expression of TNF and IL-1 increases with the degeneration and necrosis of ischemic brain tissue, and emodin can reduce the ischemic pathological damage. This effect may be achieved by inhibiting the over-expression of TNF and IL-1.