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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.