舒广文,阿尔斯拉·玉苏甫,邱韵涵,戴晨曦,邓旭坤.维吾尔药复方待比地力对顺铂所致小鼠肾损伤的保护作用[J].中南民族大学学报自然科学版,2020,39(5):478-482
维吾尔药复方待比地力对顺铂所致小鼠肾损伤的保护作用
Protective effects of DaiBiDiLi, a traditional Uighur prescription, on cisplatin-induced renal injury in mice
  
DOI:10.12130/znmdzk.20200506
中文关键词: 顺铂  肾损伤  NLRP3  维吾尔药  复方待比地力
英文关键词: cisplatin  kidney injury  NLRP3  the Traditional Uighur Medicine  DaiBiDiLi
基金项目:湖北省自然科学基金资助项目(2018CFB624)
作者单位
舒广文 中南民族大学 药学院民族药学国家级实验教学示范中心武汉 430074 
阿尔斯拉·玉苏甫 中南民族大学 药学院民族药学国家级实验教学示范中心武汉 430074 
邱韵涵 中南民族大学 药学院民族药学国家级实验教学示范中心武汉 430074 
戴晨曦 中南民族大学 药学院民族药学国家级实验教学示范中心武汉 430074 
邓旭坤 中南民族大学 药学院民族药学国家级实验教学示范中心武汉 430074 
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中文摘要:
      目的:观察维吾尔药复方待比地力(DBD)对顺铂所致小鼠肾损伤的影响. 方法:昆明小鼠40只随机分为正常组、肾损伤模型组、DBD低、高剂量干预组共4组.检测小鼠血清尿素氮(BUN)和肌酐(Cr)含量以及肾脏MDA、GSH、SOD和CAT、TNF-α、IL-1β和IL-6水平;观察肾脏显微结构;并检测肾内NOD 样受体蛋白3(NLRP3)、凋亡相关斑点样蛋白(ASC)、半胱氨酸天冬氨酸蛋白酶-1(Caspase-1)和IL-1β的蛋白表达水平. 结果:DBD能显著下调肾损伤小鼠血清中BUN和Cr的含量并改善顺铂诱导的肾脏显微结构变化. 与肾损伤模型组比较,DBD组小鼠肾内MDA水平明显降低,GSH、SOD和CAT水平则明显增加. .顺铂诱导了NLRP3、ASC和Caspase-1蛋白的表达并上调肾内炎症因子TNF-α、IL-1β和IL-6的含量. DBD剂量依赖性地改善了小鼠肾损伤. .结论:DBD能明显缓解顺铂诱导的小鼠肾损伤,其机制可能与通过抑制肾内NLRP3炎症小体各组分的表达来减轻顺铂诱导的肾脏炎症反应有关.
英文摘要:
      Objective: To observe the effect of a Traditional Uighur Prescription, DaiBiDiLi (DBD), on acute kidney injury in mice induced by cisplatin (CP). Methods: Forty Kunming mice were randomly divided into 4 groups, i.e., the normal group, the model group, the DBD low-dosage group and the DBD high-dosage group. Serum and kidneys were collected immediately. Levels of urea nitrogen (BUN), creatinine (Cr), MDA, rGSH, SOD, catalase (CAT) TNF-α, IL-1β, and interleukin-6 (IL-6) were detected. HE staining was performed to observe the microstructure of kidneys. Protein expression levels of nod-like receptor protein 3 (NLRP3), apoptosis-related spot-like protein (ASC), caspase-1, and IL-1β were determined also. Result: DBD significantly reduced levels of BUN and Cr in serum and improved the changes of renal microstructure induced by CP. The level of MDA in the kidney of DBD groups declined significantly, while levels of GSH, SOD, and CAT increased considerably. CP induced the expression of NLRP3, ASC, and caspase-1 in kidney and upregulated renal contents of TNF-α, IL-1β and IL-6. DBD ameliorated these lesions in a dose-dependent manner. Conclusion: DBD significantly alleviated CP-induced kidney injury in mice. Inhibition of the expression of NLRP3 inflammasome components to decline CP-provoked renal inflammation might be implicated in the kidney protective effect of DBD.
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