大剂量地塞米松诱导的脑细胞死亡机制
Brain cell death mechanism induced by high-dose dexamethasone
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 brain cell death mechanism induced by high-dose dexamethasone. Methods SD rats were randomly divided into the control group and the experimental group. The experimental group was divided into 7d, 9d, 11d three subgroups. The experimental group received intraperitoneal injection of DX 5mg/kg while the control group received injection with equal volume of physiological saline. light microscopy, electron microscopy, immunohistochemistry and western blot were used to observe the morphological changes of the brain tissue and detect the expression of Active Caspase-3, PARP-1, pULK1 of the brain tissue. Results (1) rat brain tissue structure was clear and normal in the control group. In the 7d experimental group, the brain tissue had no significant pathological changes. Apoptosis and oncosis of the brain cells were observed in the 11d experimental group. (2) In the control group, expression of active Caspase-3, PARP-1, pULK1 was negative. Compared with the control group, expression levels of active Caspase-3, PARP-1,pULK1 were gradually increased with the treatment time in the brain tissue of the experimental group. Conclusion Brain cell death in dexamethasone-induced may be through the activation of Caspase-3 ,PARP-1, pULK1.
地塞米松 / 脑细胞 / 半胱胺酸蛋白酶蛋白-3 / 多腺苷二磷酸核糖聚合酶 / 磷酸化自噬相关蛋白1抗体
Dexamethasone / Brain cells / Caspase3 / (ADP-ribose) polymerase / Phospho-ULK1
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