灯盏花素减轻顺铂对大鼠肾损害及肾细胞凋亡机制的研究

目的探讨应用灯盏花素减轻顺铂对大鼠肾损害及肾细胞凋亡的作用机制。方法48只SD大鼠分为对照组、模型组、25mg／kg灯盏花素组（灯盏花素1组）和50mg／kg灯盏花素组（灯盏花素2组）各12只。对照组给予羧甲基纤维素钠溶液灌胃，模型组、灯盏花素1组和2组均腹腔注射顺铂8mg／kg造模。灯盏花素1组和2组分别以25mg／kg和50mg／kg灯盏花素灌胃，给药7d后计算4组肾脏指数，采用原位缺15末端标记法检测肾细胞凋亡情况，左肾采用蛋白质印迹法检测肾皮质Bax、Bcl-2表达水平，右肾采用免疫组织化学法检测肾组织凋亡蛋白Bax和Bcl-2表达水平。结果模型组、灯盏花素1组和2组肾脏指数、凋亡指数及Bax、Bcl-2表达水平高于对照组（P〈0．05）；灯盏花素2组肾脏指数、凋亡指数、Bax表达水平及Bax／Bcl-2比值低于模型组、Bcl-2表达水平高于模型组（P〈0．05）；灯盏花素1组肾脏指数和凋亡指数高于2组（P〈0．05）。结论灯盏花素可增强凋亡蛋白Bcl-2表达、降低Bax表达，影响线粒体凋亡通路，从而减轻顺铂对肾损害大鼠肾细胞的凋亡。

Mechanism of Breviscapine in reducing cisplatin-induced kidney damage and apoptosis of kidney cells in rats

Objective To explore the mechanism of Breviscapine in reducing cisplatin-induced kidney damage and apoptosis of kidney cells. Methods Forty-eight SD rats were randomly divided into control group, model group, 25 mg/ kg Breviscapine group （Breviscapine 1 group） and 50 mg/kg Breviscapine group （Breviscapine 2 group）, with 12 rats in each group. Control group was given lavage with carboxymethylcellulose sodium, and the other three groups were established models by intraperitoneal injection of 8 mg/kg cisplatin, followed by lavage with 25 mg/kg and 50 mg/kg Breviscapine respectively in Breviscapine 1 and 2 groups. Four days later, the kidney indexes were calculated. The apoptosis indexes of kidney cells were detected by TUNEL method. The expressions of Bax and Bcl-2 in kidney cells were detected by Western blot method in the left kidney, and the expressions of Bax and Bcl-2 were detected by immunohistochemical method in the right kidney. Results The kidney indexes, apoptosis indexes, and Bax and Bcl-2 levels were higher in model group and Breviscapine groups than those in control group （P~0.01）. The kidney indexes, apoptosis indexes, Bax level and Bax/Bcl-2 were lower, and Bcl-2 level was higher in Breviscapine 2 group than that in model group （P〈0.05）. The kidney indexes and apoptosis indexes were higher in Breviscapine 1 group than those in Breviscapine 2 group （P〈 0.05）. Conclusions Breviscapine can reduce the apoptosis of kidney cells in rats with cisplatin-induced kidney damage by increasing the expression of apoptotic protein Bcl-2 and decreasing Bax expression to influence mitochondrial apoptosis pathway.