杜鹃花根对慢性肾小球肾炎大鼠模型NF-κ B活化的影响

Jing Xiong , Zhonghua Zhu , Jianshe Liu , Yang Wang
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引用次数: 11

摘要

目的探讨核因子κB (NF-κB)在慢性肾小球肾炎发病机制中的作用,并探讨杜鹃花根对NF-κB活化的影响。方法36只Wistar大鼠随机分为对照组、肾小球肾炎模型组和治疗组(杜鹃花根治疗肾小球肾炎动物)。采用皮下免疫和每日腹腔注射牛血清白蛋白(BSA)诱导牛血清白蛋白肾炎。测定24小时尿蛋白和血清肌酐值,并通过光学显微镜和电子显微镜对肾脏病理进行组织学评估。NF-κB活性测定采用电泳迁移迁移法(EMSA)。结果与对照组相比,肾小球肾炎模型大鼠24 h尿蛋白和血清肌酐均显著升高,肾脏组织学异常。杜鹃花根的添加改善了这些变化。肾小球肾炎模型组大鼠NF-κB活性高于杜鹃花治疗组,且两组大鼠NF-κB活性均高于对照组(P <0.01)。结论NF-κB参与慢性肾小球肾炎的发病机制,杜鹃花可能通过下调NF-κB的活化来减轻慢性肾小球肾炎模型的肾损害。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The effect of root of rhododendron on the activation of NF-κ B in a chronic glomerulonephritis rat model

Objective

We have explored the role of nuclear factor kappa B(NF-κB) in the pathogenesis of chronic glomerulonephritis, and investigated the effect of rhododendron root on the activation of NF-κB .

Methods

Thirty-six Wistar rats were randomly divided into three groups: a control group, a glomerulonephritis model group and a therapy group(glomerulonephritis animals treated with the root of rhododendron). Bovine serum albumin(BSA) nephritis was induced by subcutaneous immunization and daily intraperitoneal administration of BSA. Twenty-four-hour urinary protein and serum creatinine values were measured, and renal pathology was assessed histologically by optical microscopy and electron microscopy. NF-κB activity was determined by an electrophoretic mobility shift assay(EMSA).

Results

Compared with the control rats, glomerulonephritis model rats exhibited a significant increase in both 24 h urinary protein and serum creatinine, and had abnormal renal histology. The administration of the root of rhododendron ameliorated these changes. NF-κB activity in glomerulonephritis model group was greater than that in rhododendron-treated group, and NF-κB activity was greater in both glomerulonephritis groups than in the control group(P < 0.01).

Conclusion

These observations suggest that NF-κB plays a role in the pathogenesis of chronic glomerulonephritis, and rhododendron root may attenuate renal damages by downregulating the activation of NF-κ B in this model.

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