Home HOME Bratislava Medical Journal 2020 Bratislava Medical Journal Vol.121, No.11, p.822–829,2020

Journal info


 


Published Monthly, in English
Founded: 1919
ISSN 0006-9248
(E)ISSN 1336-0345

Impact factor 1.5

 

Select Journal







Webshop Cart

Your Cart is currently empty.
Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Bratislava Medical Journal Vol.121, No.11, p.822–829,2020

Title: Eicosapentaenoic acid reduces inflammation and apoptosis by SREBP1/TLR4/MYD88
Author: L. Zhang, N. N. Jia, R. H. Yang, F. Wang
Abstract: AIM: Podocytes dysfunction including the cell integrity, apoptosis and inflammation plays crucial role in diabetic nephropathy. Current exploration evaluated the protective role of eicosapentaenoic acid (EPA) in high glucose-treated podocytes and the underlying mechanisms.
METHOD: MPC5 cell were stimulated by high glucose or treated by EPA of different concentrations. CCK8 assay was utilized to assess MPC5 cell viability, flow cytometry analyzed cell apoptosis.
RESULTS: Data showed that EPA prominently alleviated the high glucose-induced apoptosis and inflammation. Besides, the disruption of the podocytes structure certifying by podocin and synaptopodin induced by hyperglycemia was hindered by EPA administration. In addition, overexpression of the sterol regulatory element-binding protein-1 (SREBP-1) reversed the protective effects of EPA in high glucose-treated podocytes. EPA inhibits the SREBP-1/TLR4/MYD88 signaling in high glucose treated cells.
CONCLUSIONS: This study suggests that EPA protects against podocytes dysfunction by regulating SREBP-1 and these findings provide a better understanding for diabetic nephropathy and a novel therapeutic strategy (Fig. 7, Ref. 24).
Keywords: eicosapentaenoic acid, inflammation, apoptosis, SREBP1/TLR4/MYD88
Published online: 09-Nov-2020
Year: 2020, Volume: 121, Issue: 11 Page From: 822, Page To: 829
doi:10.4149/BLL_2020_135


download file


© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.