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汉防己甲素对膜性肾小球肾炎 NF-κB、MCP-1 表达的影响。

Effects of sodium houttuyfonate on expression of NF-κB and MCP-1 in membranous glomerulonephritis.

机构信息

Department of Pharmacy, No. 3 People's Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 201900, China.

出版信息

J Ethnopharmacol. 2010 Aug 19;131(1):203-9. doi: 10.1016/j.jep.2010.06.020. Epub 2010 Jun 18.

Abstract

AIMS OF THE STUDY

Sodium houttuyfonate (SH) is an addition compound of sodium bisulfite and houttuynin. Houttuynin is one of the main ingredients in the volatile oil of Houttuynia cordata Thunb, which has been widely used in traditional Chinese medicines. In this study, we investigated the effect of SH in membranous glomerulonephritis (MGN) induced by cationic Bovine Serum Albumin (C-BSA) in BALB/c mice.

MATERIALS AND METHODS

Mice were divided into four groups, including normal vehicle-treated controls (N group), model (M group), low SH of 60 mg/kg body weight (L group), or high SH of 120 mg/kg body weight (H group). Urine protein quantification was detected by the urine protein strip test. Morphological assessment in kidneys was observed by light microscope and electron microscopy. The level of nuclear factor-kappaB (NF-kappaB) in the nuclear was evaluated by Western blot. Immunohistochemical was used to analyze the expression of MCP-1.

RESULTS

SH was shown to reverse C-BSA induced increases in urinary protein, and changes in morphology. Treatment with SH at 60-120 mg/kg (L and H groups, respectively) dose-dependently decreased the level of nuclear NF-kappaB and MCP-1 expression compared to that of the M group.

CONCLUSIONS

This study reveals that SH could treat C-BSA induced MGN in BALB/c mice by suppressing NF-kappaB activation and MCP-1 expression. Therefore, the most likely mechanism underlying the biological effects of SH is inhibition of an NF-kappaB mediated-cytokine pathway.

摘要

目的

硫酸氢钠祡桐碱(SH)是亚硫酸氢钠和鱼腥草素的加成化合物。鱼腥草素是蕺菜挥发油的主要成分之一,在中药中被广泛应用。本研究旨在探讨 SH 对阳离子牛血清白蛋白(C-BSA)诱导的 BALB/c 小鼠膜性肾小球肾炎(MGN)的作用。

材料与方法

将小鼠分为 4 组,包括正常对照组(N 组)、模型组(M 组)、低剂量 SH(60mg/kg 体重)组(L 组)和高剂量 SH(120mg/kg 体重)组(H 组)。采用尿蛋白试纸条检测尿蛋白定量,光镜和电镜观察肾脏形态学改变,Western blot 检测核因子-κB(NF-κB)在核内的表达,免疫组化分析单核细胞趋化蛋白-1(MCP-1)的表达。

结果

SH 可逆转 C-BSA 诱导的尿蛋白增加和形态学改变。与 M 组相比,SH 以 60-120mg/kg(L 和 H 组)剂量依赖性降低核 NF-κB 和 MCP-1 的表达。

结论

本研究表明,SH 可能通过抑制 NF-κB 激活和 MCP-1 表达来治疗 C-BSA 诱导的 BALB/c 小鼠 MGN。因此,SH 的生物学效应的最可能机制是抑制 NF-κB 介导的细胞因子途径。

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