Cordyceps militaris fruit body extract ameliorates membranous glomerulonephritis by attenuating oxidative stress and renal inflammation via the NF-κB pathway
Cordyceps militaris fruit body extract ameliorates membranous glomerulonephritis by attenuating oxidative stress and renal inflammation via the NF-κB pathway
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DOI：
10.1039/c5fo01017a
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发表时间：
2016-01-01
期刊：
影响因子：
6.1
通讯作者：
Wang, Di
中科院分区：
文献类型：
--
作者：
Song, Jingjing;Wang, Yingwu;Wang, Di
膜性肾小球肾炎（MGN）是成人肾病综合征的常见发病机制。核因子-κ B（NF-κ B）是炎症反应介导的肾病的主要转录因子。蛹虫草含有多种药理活性成分，是一种具有提高免疫力、抗炎作用的生药和民间滋补食品。本研究旨在探讨蛹虫草水提物（CM）对阳离子牛血清白蛋白（C-BSA）诱导的大鼠膜性肾小球肾炎模型的肾脏保护作用。MGN大鼠肾功能明显受损，CM给药4周后，24 h尿蛋白、总胆固醇、甘油三酯、血尿素氮、血清肌酐明显下降，血清白蛋白、总蛋白明显升高。引人注目的是，在CM处理的MGN大鼠中注意到肾组织结构的恢复。一个显着的改善谷胱甘肽过氧化物酶和超氧化物歧化酶的水平，并降低丙二醛浓度观察到CM处理的大鼠的血清和肾脏。CM治疗后，炎症细胞因子（包括白介素、单核细胞趋化蛋白-1、细胞间粘附分子1、血管粘附分子1、肿瘤坏死因子-α、6-酮-前列腺素F1 α和核转录因子亚单位NF-κ B p65）水平的改变恢复至正常水平。目前的数据表明，CM通过正常化NF-κ B B活性，从而抑制氧化损伤和降低炎症细胞因子水平，从而保护大鼠免受膜性肾小球肾炎，这进一步提供了实验证据，支持CM作为一种有效的肾脏保护剂的临床应用。
Membranous glomerulonephritis (MGN) is a common pathogenesis of nephritic syndrome in adult patients. Nuclear factor kappa B (NF-kappa B) serves as the main transcription factor for the inflammatory response mediated nephropathy. Cordyceps militaris, containing various pharmacological components, has been used as a kind of crude drug and folk tonic food for improving immunity and reducing inflammation. The current study aims to investigate the renoprotective activity of Cordyceps militaris aqueous extract (CM) in the cationic bovine serum albumin (C-BSA)-induced rat model of membranous glomerulonephritis. Significant renal dysfunction was observed in MGN rats; comparatively, 4-week CM administration strongly decreased the levels of 24 h urine protein, total cholesterol, triglyceride, blood urea nitrogen and serum creatinine, and increased the levels of serum albumin and total serum protein. Strikingly, recovery of the kidney histological architecture was noted in CM-treated MGN rats. A significant improvement in the glutathione peroxidase and superoxide dismutase levels, and a reduced malondialdehyde concentration were observed in the serum and kidney of CM-treated rats. Altered levels of inflammatory cytokines including interleukins, monocyte chemoattractant protein-1, intercellular adhesion molecule 1, vascular adhesion molecule 1, tumor necrosis factor-alpha, 6-keto-prostaglandin F1 alpha, and nuclear transcriptional factor subunit NF-kappa B p65 reverted to normal levels upon treatment with CM. The present data suggest that CM protects rats against membranous glomerulonephritis via the normalization of NF-kappa B activity, thereby inhibiting oxidative damage and reducing inflammatory cytokine levels, which further provide experimental evidence in support of the clinical use of CM as an effective renoprotective agent.