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抑制纤维连接蛋白表达对瑞宁治疗 IgA 肾病大鼠的保护作用。

Protection of rhein on IgA nephropathy mediated by inhibition of fibronectin expression in rats.

机构信息

Department of Graduate School, Medical College of Nanchang University, Nanchang, China.

出版信息

Indian J Pharmacol. 2013 Mar-Apr;45(2):174-9. doi: 10.4103/0253-7613.108309.

DOI:10.4103/0253-7613.108309
PMID:23716895
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3660931/
Abstract

OBJECTIVE

To investigate the protective effects of rhein on IgA nephropathy (IgAN) in the rat model.

MATERIALS AND METHODS

Twenty-eight female sprague dawley rats were divided randomly into four groups, namely control, IgAN, rhein-prevented and rhein-treated. The pathologic changes on renal tissue were observed by the H and E, staining and the amount of urinary red blood cells and 24-h urinary protein excretion were measured. The glomerular deposition of immune globulin A (IgA) was measured by immunofluorescence staining. Fibronectin (FN) and α-smooth muscle actin (α-SMA) expression on renal tissue were measured via immunohistochemistry.

RESULTS

The model of IgAN was established according to Bovine serum albumin-Lipopolysaccharide-Carbon tetrachloride protocol, which was evidenced by histological structural lesions of glomeruli, IgA deposition and urinary measurement. Histological examination of kidney sections from both rhein-prevented group and rhein-treated group showed that glomerular hypertrophy, mesangial expansion, excessive extracellular matrix, and renal capsule dilation were markedly ameliorated compared with IgAN group. Moreover, rhein treatment significantly reduced IgA deposition in glomerulus, the volume of urinary red blood cells and 24-h urinary protein excretion. More importantly, increased FN expression in IgAN was back to normal level in rhein-prevented and rhein-treated group, which was along with the reduction of α-SMA expression in renal tissues.

CONCLUSIONS

These findings indicate that rhein prevents the development of glomerulosclerosis and halts the progression of IgAN via inhibition of FN and α-SMA expression.

摘要

目的

探讨大黄酸对 IgA 肾病(IgAN)大鼠模型的保护作用。

材料与方法

将 28 只雌性 Sprague-Dawley 大鼠随机分为 4 组,分别为对照组、IgAN 组、大黄酸预防组和大黄酸治疗组。通过 H&E 染色观察肾脏组织的病理变化,测量尿红细胞数和 24 小时尿蛋白排泄量。免疫荧光染色法检测肾小球免疫球蛋白 A(IgA)沉积。免疫组化法检测肾脏组织中纤维连接蛋白(FN)和α-平滑肌肌动蛋白(α-SMA)的表达。

结果

采用牛血清白蛋白-脂多糖-四氯化碳方案成功建立 IgAN 模型,表现为肾小球结构损伤、IgA 沉积和尿液检测异常。大黄酸预防组和治疗组的肾脏组织切片的组织学检查显示,与 IgAN 组相比,肾小球肥大、系膜扩张、细胞外基质过度沉积和肾包膜扩张明显改善。此外,大黄酸治疗显著减少了肾小球中 IgA 的沉积、尿红细胞数和 24 小时尿蛋白排泄量。更重要的是,IgAN 中 FN 表达的增加在大黄酸预防组和治疗组恢复正常水平,同时肾脏组织中 α-SMA 表达减少。

结论

这些发现表明,大黄酸通过抑制 FN 和 α-SMA 的表达,预防肾小球硬化的发展并阻止 IgAN 的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bae/3660931/1dafeab08ece/IJPharm-45-174-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bae/3660931/7686e558cac1/IJPharm-45-174-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bae/3660931/190788d9f3db/IJPharm-45-174-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bae/3660931/99b125aafcc9/IJPharm-45-174-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bae/3660931/1dafeab08ece/IJPharm-45-174-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bae/3660931/7686e558cac1/IJPharm-45-174-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bae/3660931/190788d9f3db/IJPharm-45-174-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bae/3660931/99b125aafcc9/IJPharm-45-174-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bae/3660931/1dafeab08ece/IJPharm-45-174-g007.jpg

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