文章摘要
于 平,董文培,陆 菲,何 萱,卞晓岚,陆嘉君.维生素C对万古霉素诱导大鼠肾损伤自噬的作用[J].,2022,(7):1201-1205
维生素C对万古霉素诱导大鼠肾损伤自噬的作用
Inhibitory Effect of Vitamin C on the Level of Autophagy in Vancomycin-induced Rat Renal Injury
投稿时间:2021-12-12  修订日期:2021-12-30
DOI:10.13241/j.cnki.pmb.2022.07.001
中文关键词: 万古霉素  肾损伤  维生素C  自噬
英文关键词: Vancomycin  Kidney injury  Vitamin C  Autophagy
基金项目:国家自然科学基金项目(81970455);中国毒理学会临床毒理专项(CST2019CT301);北京康盟慈善基金会医学科研发展基金项目(HS202001)
作者单位E-mail
于 平 上海交通大学医学院附属瑞金医院药剂科 上海 200025 zjypwz@163.com 
董文培 复旦大学附属华东医院普外科 上海 200040  
陆 菲 上海交通大学医学院附属瑞金医院药剂科 上海 200025  
何 萱 上海交通大学医学院附属瑞金医院药剂科 上海 200025  
卞晓岚 上海交通大学医学院附属瑞金医院药剂科 上海 200025  
陆嘉君 上海交通大学医学院附属瑞金医院药剂科 上海 200025  
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中文摘要:
      摘要 目的:探讨维生素C对万古霉素诱导肾损伤自噬水平的影响。方法:将20只雄性SD大鼠随机分为:对照组、万古霉素组、万古霉素+维生素C组和维生素C组。万古霉素组:连续每天腹腔注射400 mg/kg万古霉素;万古霉素+维生素C组:注射万古霉素之前30 min腹腔注射200 mg/kg维生素C;对照组和维生素C组分别单独注射同体积的生理盐水和200 mg/kg维生素C。连续给药7 d后,通过苏木精-伊红染色(HE)观察大鼠肾组织病理损伤;免疫组化和免疫荧光检测肾组织中LC3B和Beclin 1的表达情况,比较各组之间的表达差异。结果:相对于对照组,万古霉素诱导大鼠肾损伤模型组肾组织出现明显的病理改变,包括肾间质水肿,肾小管细胞质空泡性变化,细胞凋亡坏死等;同时观察到肾组织中LC3B光密度明显升高和Beclin 1的荧光强度显著增强。维生素C处理组,肾组织的病理损伤显著改善并且自噬相关蛋白LC3B和Beclin 1的表达显著降低。相对于对照组,维生素C单独处理组肾组织损伤和自噬相关蛋白的表达无明显变化。结论:维生素C可降低自噬相关蛋白LC3B和Beclin 1的表达,缓解万古霉素诱导的大鼠肾损伤。
英文摘要:
      ABSTRACT Objective: To investigate the effect of vitamin C on the changes of autophagy in vancomycin-induced rat renal injury. Methods: 20 male SD rats were randomly divided into control group, vancomycin group, vancomycin plus vitamin C group and vitamin C group. Vancomycin group was treated with continuous daily intraperitoneal injection of 400 mg/kg vancomycin. Vancomycin + vitamin C group was intraperitoneally injected with 200 mg/kg vitamin C 30 min before vancomycin. Control group and vitamin C group were separately injected with the same volume of normal saline and 200 mg/kg vitamin C. After 7 days' continuous administration, the pathological damage of kidney tissue was observed by hematoxylin-eosin (HE) staining. The expression of LC3B and Beclin 1 in renal tissues was detected by immunohistochemistry and immunofluorescence. Results: Compared with the control group, obvious renal pathological damage in model group was found including renal interstitial edema, vacuolar change of renal tubule cytoplasm, apoptosis and necrosis. Meanwhile, the integral optical density of LC3B and the fluorescence intensity of Beclin 1 were significantly increased in renal tissue. In the vitamin C plus vancomycin treatment group, the pathological injury of renal tissue was significantly improved and the expression of autophagy related proteins LC3B and Beclin 1 was significantly decreased. Compared with the control group, there were no significant difference in the renal pathological change and the expression of autophagy related proteins in the group of vitamin C treated alone. Conclusion: Vitamin C could reduce the expression of autophagy related proteins LC3B and Beclin 1, and alleviate vancomycin- induced rat renal injury.
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