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目的:观察灯盏花素对顺铂致小鼠肾损害肾组织细胞凋亡及相关蛋白的影响。方法:将昆明种小鼠随机分为对照组、模型组、灯盏花素25,50 mg.kg-1组。除对照组外,其余各组腹腔注射顺铂8 mg.kg-1制备小鼠肾损害模型,灯盏花素组分别灌胃给药,连续7 d。给药结束后收集小鼠尿液进行尿蛋白(Upr)/尿肌酐(Ucr)及N-乙酰-β-D-氨基葡萄糖苷酶(NAG-U)测定。原位末端标记法(TUNEL)检测小鼠肾脏细胞凋亡状况,免疫组化法检测肾脏相关凋亡蛋白Bax和Bcl-2的表达。结果:模型组小鼠Upr/Ucr及NAG-U较对照组明显升高,肾组织的凋亡指数增加,肾组织细胞凋亡蛋白Bax及Bcl-2表达增强,Bax/Bcl-2比值升高(P<0.05,P<0.01),而2个灯盏花素实验组Upr/Ucr、NAG-U较模型组明显降低(P<0.05,P<0.01),其中灯盏花素50 mg.kg-1小鼠较模型组肾组织细胞凋亡指数、Bax表达、Bax/Bcl-2减少,Bcl-2的表达增强(P<0.05,P<0.01)。结论:Upr/Ucr与NAG-U可作为顺铂肾损害的评估指标。灯盏花素减轻顺铂肾损害的机制可能与增强凋亡相关蛋白Bcl-2的表达,降低Bax表达及Bax/Bcl-2的比值有关。
Objective: To observe the effect of breviscapine on renal cell apoptosis and its related proteins induced by cisplatin in mice. Methods: Kunming mice were randomly divided into control group, model group, breviscapine 25,50 mg.kg-1 group. In addition to the control group, the other groups were intraperitoneally injected cisplatin 8 mg.kg-1 mouse model of renal damage, breviscapine group were administered orally for 7 days. Urine was collected from the urine of mice for determination of urinary protein (Ur), urinary creatinine (Ucr) and N-acetyl-β-D-glucosaminidase (NAG-U) TUNEL assay was used to detect the apoptosis of mouse kidney cells and the expressions of Bax and Bcl-2 were detected by immunohistochemistry. Results: Upr / Ucr and NAG-U in model group were significantly higher than those in control group, and the apoptotic index in renal tissue was increased, while the expression of Bax and Bcl-2 in renal tissue was increased and the ratio of Bax / Bcl-2 was increased (P <0.05, P <0.01), but Upr / Ucr and NAG-U in two breviscapine groups were significantly lower than those in the model group (P <0.05, P <0.01). Breviscapine 50 mg.kg-1 Compared with model group, the apoptosis index, Bax, Bax / Bcl-2 and the expression of Bcl-2 in renal tissue of mice increased (P <0.05, P <0.01). Conclusion: Upr / Ucr and NAG-U can be used as indicators of renal damage of cisplatin. Breviscapine reduce the mechanism of renal damage of cisplatin may be related to increasing the expression of apoptosis-related protein Bcl-2, decreasing Bax expression and Bax / Bcl-2 ratio.