#4313 AN ANTI-FIBROTIC GENE ATTENUATES DIABETIC KIDNEY INJURY IN DB/DB MICE BY INHIBITING FIBROSIS VIA EPITHELIAL-MESENCHYMAL TRANSITION PATHWAY

Abstract Background and Aims Diabetic nephropathy (DN) is a major cause of mortality in patients with diabetes chronic kidney disease, but there lack effective therapeutic drugs for this disease. The development progression DN influenced by fibrosis. transforming growth factor (TGF)-β1 key cytokine involved fibrosis many different organ systems. Anti-fibrotic gene (Anti-F) TGF-β/Smad signaling. Here we examined the effect Anti-F model using db/db mice streptozotocin (STZ) treatment. Method were divided into five groups; db/m+ (wild type), db/db+saline, db/db+STZ, db/db+STZ+CMV-Anti-F, db/db+STZ+TGF-β-Anti-F. STZ was peritoneally injected consecutive days (50mg/kg) (40μg/head) administered once every two weeks. Mice sacrificed four months after injection. Results CMV TGF-β promoter administration markedly alleviated metabolic syndrome assessed obesity hyperglycemia, renal dysfunction overweight albuminuria db/db+STZ mice. obviously mitigated glomerular damage diabetic mice, as reflected reduction increased mesangial expansion expression nephrin podocin Additionally, interstitial also significantly inhibited through suppressing epithelial-mesenchymal transition (EMT) signaling including α-SMA, Twist, Snail, well inflammation IL-1β, MMP-2, MMP-9 Conclusion attenuated type 2 diabetes. protective associated decreased subsequent attenuation EMT-mediated Thus, study suggests that targeting could be considered novel approach preventing DN.