灵芝多糖对糖尿病肾病小鼠肾小管上皮细胞间充质转化的抑制作用

Abstract
Figure/Table
References (24)
Related Citation (15)

Download: PDF (785 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the effect of ganoderma lucidum polysaccha-ride (GLP) on epithelial-to-mysenchymal transition (EMT) of renal tubular epithelial cells in diabetic nephropathy (DN) mice. Methods Forty C57BL/KsJ-db/db mice were randomly divided into 5 groups by weight. Normal group was fed with normal feed. Model group, GLP low (100 mg/kg), high (400 mg/kg) dose groups and Irbesartan group (50 mg/kg, Irbesartan) were given high-sugar dieat. Each group was given the drug by gavage daily for 8 weeks after successful modeling of DN mice. The changes of renal function, blood lipid and other physiological indexes were measured. The protein expression and mRNA level of E-cadherin, α-SMA, TGF-β1, Fibronectin, Vimentin, N-cadherin, TGF-β1, p-Smad2, p-Smad3, Smad2 and Smad3 were measured by Western Blot and Real-time PCR. Results Compared with the model group, the renal function and blood lipid metabolism in GLP low and high doses group were significantly decreased (P ＜ 0.05). Compared with the model group, the levels of E-cadherin protein and mRNA were increased in the GLP low and high doses group and the Irbesartan group, while the levels of α-SMA, Fibronectin, Vimentin, N-cadherin protein and mRNA were decreased (P ＜ 0.01). The expression levels of Smad2 and Smad3 were unchanged. Conclusion GLP inhibits EMT maybe via inhibition of TGF-β1/Smad signaling pathway.

Key words： Ganoderma lucidum polysaccharide Endothelial to mesenchymal transition Diabetic nephropathy TGF-β1/Smad signaling pathway

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	ZHONG Tao1 ZHANG Guoxin1 ZHOU Diyi2 ZHU Tiane1▲

Cite this article:

ZHONG Tao1 ZHANG Guoxin1 ZHOU Diyi2 ZHU Tiane1▲. Inhibitory effect of ganoderma lucidum polysaccharide on renal tubular endothelial-to-mesenchymal transition of diabetic nephropathy mice[J]. 中国医药导报, 2020, 17(6): 9-12.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2020/V17/I6/9

[1] 沈义兰，丁涛，梅小斌. 糖尿病肾病的生物治疗及研究进展[J].药学服务与研究，2018，18（6）：401-405.
[2] 孙迎春，解汝娟.糖尿病肾病发病机制的研究进展[J].医学综述，2017，23（16）：3286-3290.
[3] Nangaku M. Mechanisms of tubulointerstitial injury in the kidney：final common pathways to end-stage renal failure [J]. Intern Med，2004，43（1）：9-17.
[4] Thomas MC，Burns WC，Cooper ME. Tubular changes in early diabetic nephropathy [J]. Adv Chronic Kidney Dis，2005，12（2）：177-186.
[5] Venkov CD，Link AJ，Jennings JL，et al. A proximal activator of transcription in epithelial-mesenchymal transition [J]. J Clin Invest，2007，117（2）：482-491.
[6] Willis BC，Borok Z. TGF-beta-induced EMT：mechanisms and implications for fibrotic lung disease [J]. Am J Physiol Lung Cell Mol Physiol，2007，293（3）：L525-L534.
[7] 陈文华，程显好，谭会颖，等.灵芝多糖的药理作用及其机制研究进展[J].中国药房，2018，29（24）：3446-3450.
[8] 刘亚萍，张泽生，李雨蒙，等.灵芝多糖降血糖机制的研究进展[J].食品研究与开发，2018，39（2）：215-218.
[9] Wilson PG，Thompson JC，Yoder MH，et al. Prevention of renal apoB retention is protective against diabetic nephropathy：role of TGF-beta inhibition [J]. J Lipid Res，2017，58（12）：2264-2274.
[10] 何其英.基于TGF-β-1-Smad2/3探讨芪地糖肾颗粒防治糖尿病肾病肾脏纤维化的研究[D].北京：北京中医药大学，2018.
[11] 吴航，孙子林.糖尿病肾病的发病机制和药物干预研究进展[J].药学进展，2016，40（5）：337-343.
[12] 柳俊辉，龚小妹，周小雷，等.西瓜藤乙酸乙酯提取物对糖尿病肾病大鼠肾小管的保护作用[J].中国药学杂志，2014，49（24）：2173-2176.
[13] 梁航.血脂与2型糖尿病肾病进展相关性分析[C].中国中西医结合学会肾脏疾病专业委员会2018年学术年会论文.出版地：重庆，中国中西医结合学会肾脏疾病专业委员会：中国中西医结合学会，2018：1681.
[14] 毛雨河，李文，薛少清，等.糖尿病肾病患者终末期心脏结构与功能的超声心动图表现观察与分析[J].中国医药科学，2018，8（19）：244-246.
[15] Phukan RR，Goswami RK. Unusual Dyslipidemia in Patients with Chronic Kidney Diseases [J]. J Clin Diagn Res，2017，11（1）：C1-C4.
[16] 陆鸣，夏宁，梁瑜祯.TGF-β/smad信号通路在糖尿病肾病中的作用[J].国外医学·内分泌学分册，2005（2）：131-133.
[17] 贾岳岳，汪晓霞.核因子E2相关因子2与糖尿病肾病相关研究进展[J].医学综述，2018，24（10）：2038-2042.
[18] Qi W，Chen X，Poronnik P，et al. The renal cortical fibroblast in renal tubulointerstitial fibrosis [J]. Int J Biochem Cell Biol，2006，38（1）：1-5.
[19] Liu L，Wang Y，Yan R，et al. Oxymatrine Inhibits Renal Tubular EMT Induced by High Glucose via Upregulation of SnoN and Inhibition of TGF-beta1/Smad Signaling Pathway [J]. PLoS One，2016，11（3）：e151986.
[20] Kawai T，Masaki T，Doi S，et al. PPAR-gamma agonist attenuates renal interstitial fibrosis and inflammation through reduction of TGF-beta [J]. Lab Invest，2009，89（1）：47-58.
[21] Sato M，Muragaki Y，Saika S，et al. Targeted disruption of TGF-beta1/Smad3 signaling protects against renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction [J]. J Clin Invest，2003，112（10）：1486-1494.
[22] 贾会玉，李中南，陈光亮. 糖尿病肾病中转化生长因子β1/Sma和Mad相关蛋白信号通路的作用及其相关药物研究进展[J].中国药理学与毒理学杂志，2016，30（3）：266-271.
[23] 黄琦，廖鑫，王攀，等.2型糖尿病肾病患者血清趋化素与胱抑素C水平的相关性[J].成都医学院学报，2019， 14（6）：732-735.
[24] Esmaeili N，Ebrahimzadeh H，Abdi K. Correlation Between Polyphenol Oxidase （PPO） Activity and Total Phenolic Contents in Crocus sativus L. Corms During Dormancy and Sprouting Stages [J]. Pharmacogn Mag，2017， 13（Suppl 3）：S519-S524.