Diabetes Meeting 2018: Impact of liquiritigenin on apoptotic beta-cell death by palmitate-incited lipotoxicity in INS-1 cells- Gong Deuk Bae- Eulji University

Actuation of estrogen receptor flagging assumes a significant job to save useful betaâcell mass in treatment of diabetes. Liquiritigenin (LQ), a flavonoid confined from Glycyrrhiza uralensis, is an estrogenic compound which goes about as an agonist for the estrogen receptor β. In this examination, we researched defensive impact of LQ on palmitate (Dad)- prompted apoptosis in INS-1 cells. Strategies: To look at impact of LQ on beta cells, glucose invigorated insulin emission (GSIS) by catalyst immunoassay (EIA) technique and cell suitability by MTT were estimated in rodent beta-cell line INS-1 cells. To instigate lipotoxicity, Dad (400 μM) was treated for 24 h and measure of apoptotic cells were examined utilizing a stream cytometer with annexin-V recoloring. Articulation level of apoptotic proteins and endoplasmic reticulum (ER) stress markers were dissected by western blotch investigation after LQ treatment. Tunicamycin and thapsigargin were utilized to ER stress inducer and AKT inhibitor (AKTi-1/2) was utilized to hinder LQ-prompted AKT phosphorylation at ser 473. Results: Presentation of INS-1 cells to 5 μM of LQ altogether expanded GSIS just as cell feasibility. Dad treatment expanded annexin-V recolored cells and apoptotic proteins, for example, separated caspase-3, cut poly (ADP-ribose) polymerase and bax, however these increments were essentially hindered by LQ treatment. LQ treatment restrained cell demise by ER stress inducers and Dad incited ER stress marker proteins, for example, Cleave and phosphorylated types of Advantage and eIF2α was likewise fundamentally downregulated in LQ rewarded cells.

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