Rutin reduces inflammation and fibrosis via TGF‐β/SMAD pathways in IgA nephropathy induced rats

Author:

Jash Rajiv12ORCID,Maji Himangshu Sekhar1,Chowdhury Arnab3,Biswas Sayak3,Maparu Kousik2,Khatun Robina2,Dey Suddhasattya2

Affiliation:

1. Department of Pharmaceutical Sciences JIS University Kolkata India

2. Department of Pharmaceutical Sciences Sanaka Educational Trust's Group of Institutions Durgapur West Bengal India

3. Department of Pathology Shri Ramkrishna Institute of Medical Sciences and Sanaka Hospital Durgapur West Bengal India

Abstract

AbstractAimRutin is a flavonoid glycoside obtained from the plant Ruta graveolens. It was known to have immunosuppressant activities. This study was focused on effect of rutin against immunoglobulin A (IgA) nephropathy.MethodsIgA nephropathy was induced in Sprague–Dawley rats with various inducing agents described in text. During the later part of the induction phase, rutin was administered. Control group rats did not receive any treatment or inducing agent, induced group rats received only the inducing agents, whereas treatment group received the inducing agents as well as rutin.ResultsDuring the study, various biochemical parameters pertaining to kidney function were evaluated and also, the expression of proteins and cytokines responsible for inflammation and fibrosis were assessed. The effect of rutin in IgA nephropathy was promising as treatment with rutin reduced the deposition of IgA in the glomeruli of rats. Along with this we also tried to establish the probable mechanism of action of rutin and based on the summary of the results it was concluded that rutin reduced the inflammation and fibrosis related to IgA nephropathy by inhibiting the TGF‐β/SMAD pathways and ultimately reducing the expression of α‐smooth muscle actin (α‐SMA).ConclusionComprehending all the above consideration, it may be safely said that that rutin alleviated inflammation and also fibrosis mediated by IgA, by suppressing the transforming growth factor‐β (TGF‐β) activities through suppressor of mothers against decapentaplegic pathways and reduced the epithelial‐to‐mesenchymal transition by downregulating the α‐SMA which is a marker for fibrosis.image

Publisher

Wiley

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