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目的:探讨化瘀导滞汤防治庆大霉素所致肾毒性损伤的作用和部分机理。方法:18只健康雄性W ister大鼠随机分为3组,每组6只:正常组、模型组、治疗组。给予庆大霉素造成肾毒性损伤,于造模后5天取材,光镜和电镜下观察肾组织形态学改变,计算肾系数、检测血肌酐、血尿素氮、24h尿蛋白总量,氧化应激相关指标SOD、MDA、NOS的变化,检测NF-кB蛋白表达水平。结果:模型组大鼠与正常组比较:光镜下可见肾小管上皮细胞以变性为主,部分坏死;有较多的蛋白管型和少量的细胞管型、颗粒管型。电镜下可见肾小管上皮细胞胞浆中有大量脂滴存在,细胞的线粒体肿胀、内质网明显扩张,治疗组病变轻于模型组。模型组肾系数、血肌酐、血尿素氮、24h尿蛋白总量、NF-кB蛋白表达水平以及MDA、NOS明显高于正常组,SOD明显低于正常组(P<0.01),治疗组除24h尿蛋白总量外,其余指标与模型组相比有明显改善(P<0.01)。结论:化瘀导滞汤有良好的防治庆大霉素所致肾毒性损伤的作用,并提示与早期抗脂质过氧化损伤有关。
Objective: To investigate the effect and mechanism of Huayu Zhizhi Decoction in preventing and treating nephrotoxicity induced by gentamicin. Methods: Eighteen healthy male wistar rats were randomly divided into 3 groups, 6 in each group: normal group, model group and treatment group. Renal toxicity was induced by gentamicin. Morphological changes of renal tissue were observed under light microscope and electron microscope. The renal coefficient was calculated. Serum creatinine, blood urea nitrogen, 24-hour urinary protein, The correlation indexes of SOD, MDA and NOS were measured to detect the expression of NF-κB protein. Results: Compared with the normal group, the model group showed that the renal tubular epithelial cells were mainly degenerative and partially necrotic under the light microscope; there were more protein tubes and a few of cell tube and granular tube. Electron microscopy showed a large number of lipid droplets in the cytoplasm of renal tubular epithelial cells, mitochondria swelling cells, endoplasmic reticulum was significantly expanded, the treatment group lesions lighter than the model group. The renal coefficient, serum creatinine, blood urea nitrogen, 24-hour urinary protein, NF-кB protein expression and MDA and NOS in the model group were significantly higher than those in the normal group, and SOD was significantly lower than the normal group (P <0.01) Urine protein, the remaining indicators were significantly improved compared with the model group (P <0.01). Conclusion: Huayu Zhixue Decoction has a good effect on prevention and treatment of gentamicin-induced nephrotoxicity and suggests that it is related to early anti-lipid peroxidation injury.