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目的探讨大剂量地塞米松诱导的大鼠的脑细胞死亡机制。方法将SD大鼠分为对照组和实验组(包括7、9、11 d,3个时间点)。对照组腹腔注射生理盐水,实验组连续腹腔注射5 mg/kg地塞米松,每日1次。利用光镜和电镜技术观察大脑组织形态结构变化,采用免疫组化和免疫印迹方法检测大脑顶叶皮质Active Caspase-3、PARP-1、pULK1的表达情况。结果 (1)对照组大鼠大脑组织结构清晰,脑细胞排列整齐,形态完整,染色清晰;7d实验组大鼠大脑组织未见明显病理改变;9d实验组部分脑细胞死亡;11d实验组部分脑细胞可见凋亡和胀亡。(2)对照组Active Caspase-3、PARP-1、pULK1均呈阴性表达。与对照组比较,实验组脑细胞胞质内可见明显的Active Caspase-3、pULK1表达,细胞核内可见明显的PARP-1阳性表达,各实验组脑组织内Active Caspase-3、PARP-1、pULK1表达量随着处理时间的延长而增高。结论地塞米松诱导的脑细胞死亡可能通过Active Caspase-3、PARP-1、pULK1的活化所致。
Objective To investigate the mechanism of brain cell death induced by high-dose dexamethasone in rats. Methods SD rats were divided into control group and experimental group (including 7, 9, 11 d, 3 time points). The control group was injected intraperitoneally with saline, and the experimental group was given 5 mg / kg dexamethasone once a day by intraperitoneal injection. The morphological changes of brain tissue were observed by light microscope and electron microscope. The expressions of active Caspase-3, PARP-1 and pULK1 in parietal cortex were detected by immunohistochemistry and immunoblotting. Results: (1) The brain tissue of rats in the control group had a clear structure and organized brain cells with complete morphology and clear staining. No significant pathological changes were observed in the brain tissue of the rats in the experimental group for 7 days; some brain cells died in the experimental group on the 9th day; Cell apoptosis and expansion can be seen. (2) The control group, Active Caspase-3, PARP-1, pULK1 were negative expression. Compared with the control group, significant expression of Active Caspase-3 and pULK1 was observed in the cytoplasm of brain cells in experimental group, and significant positive expression of PARP-1 in nucleus was observed in experimental group. Active Caspase-3, PARP-1, pULK1 The expression increased with the prolongation of treatment time. Conclusion Dexamethasone-induced brain cell death may be caused by the activation of active Caspase-3, PARP-1 and pULK1.