Epigenetic modulation of autophagy genes linked to diabetic nephropathy by administration of isorhamnetin in Type 2 diabetes mellitus rats
Matboli, Marwa; Ibrahim, Doaa; Hasanin, Amany H.; Hassan, Mohamed K.; Habib, Eman K.; Bekhet, Miram M.; Afifi, Ahmed M.; Eissa, Sanaa;
Abstract
Aim: To assess isorhamnetin efficacy for diabetic kidney disease in a Type 2 diabetes mellitus rat model, through investigating its effect at the epigenetic, mRNA and protein levels. Materials & methods: Type 2 diabetes mellitus was induced in rats by streptozotocin and high-fat diet. Rats were treated with isorhamnetin (50 mg/kg/d) for 4 or 8 weeks. Fasting blood glucose, renal and lipid profiles were evaluated. Renal tissues were examined by light and electron microscopy. Autophagy genes (FYCO1, ULK, TECPR1 and WIPI2) and miR-15b, miR-34a and miR-633 were assessed by qRT-PCR, and LC3A/B by immunoblotting. Results: Isorhamnetin improved fasting blood glucose, renal and lipid profiles with increased autophagosomes in renal tissues. It suppressed miRNA regulation of autophagy genes. Conclusion: We propose a molecular mechanism for the isorhamnetin renoprotective effect by modulation of autophagy epigenetic regulators.
Other data
Title | Epigenetic modulation of autophagy genes linked to diabetic nephropathy by administration of isorhamnetin in Type 2 diabetes mellitus rats | Authors | Matboli, Marwa ; Ibrahim, Doaa; Hasanin, Amany H.; Hassan, Mohamed K.; Habib, Eman K.; Bekhet, Miram M.; Afifi, Ahmed M.; Eissa, Sanaa | Keywords | autophagy;bioinformatics;diabetic nephropathy;epigenetics;flavonoid plants;isorhamnetin;miRNA;RNA;rtPCR;western blot | Issue Date | 7-Jan-2021 | Publisher | FUTURE MEDICINE LTD | Journal | Epigenomics | Volume | 13 | Issue | 3 | ISSN | 17501911 | DOI | 10.2217/epi-2020-0353 | PubMed ID | 33406900 | Scopus ID | 2-s2.0-85101096094 | Web of science ID | WOS:000605602900001 |
Recommend this item
Similar Items from Core Recommender Database
Items in Ain Shams Scholar are protected by copyright, with all rights reserved, unless otherwise indicated.