Emodin ameliorates high glucose induced-podocyte epithelial-mesenchymal transition in-vitro and in-vivo

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
Tingfang ChenNiansong Wang

Abstract

Epithelial-to-mesenchymal transition (EMT) is a potential pathway leading to podocyte depletion and proteinuria in diabetic kidney disease (DKD). Here, we investigated the protective effects of Emodin (EMO) on high glucose (HG) induced-podocyte EMT in-vitro and in-vivo. Conditionally immortalized mouse podocytes were exposed to HG with 30 μg /ml of EMO and 1 μmol/ml of integrin-linked kinase (ILK) inhibitor QLT0267 for 24 h. Streptozotocin (STZ)-induced diabetic rats were treated with EMO at 20 mg· kg(-1)· d(-1) and QLT0267 at 10 mg· kg(-1)· w(-1) p.o., for 12 weeks. Albuminuria and blood glucose level were measured. Immunohistochemistry, immunofluorescence, western blotting and real-time PCR were used to detect expression of ILK, the epithelial marker of nephrin and the mesenchymal marker of desmin in-vitro and in-vivo. HG increased podocyte ILK and desmin expression while decreased nephrin expression. However, EMO significantly inhibited ILK and desmin expression and partially restored nephrin expression in HG-stimulated podocytes. These in-vitro observations were further confirmed in-vivo. Treatment with EMO for 12 weeks attenuated albuminuria, renal histopathology and podocyte foot process effacement in diabetic rats. EMO a...Continue Reading

Citations

Aug 31, 2016·Nature Reviews. Nephrology·Luca PericoGiuseppe Remuzzi
May 18, 2016·Phytotherapy Research : PTR·Xiaoxv DongJian Ni
Nov 28, 2019·Phytotherapy Research : PTR·Aminu MohammedMurtala Bindawa Isah
Oct 28, 2019·International Journal of Molecular Sciences·Marco CalvarusoLuigi Minafra
Jul 23, 2020·Journal of Diabetes Research·Lili ZhangXiaolin Tong
Jul 1, 2021·Néphrologie & thérapeutique·Yue QiuChun Zhang

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