TY - JOUR ID - 250459 TI - Punica granatum L. Fruit Aqueous Extract Suppresses Reactive Oxygen Species-Mediated p53/p65/miR-145 Expressions followed by Elevated Levels of irs-1 in Alloxan-Diabetic Rats JO - Cell Journal (Yakhteh) JA - CELLJ LA - en SN - 2228-5806 AU - Gharib, Ehsan AU - Kouhsari, Shideh Montasser AU - Izad, Maryam AD - Department of Cellular and Molecular Biology, School of Biology, University College of Science, University of Tehran, Tehran, Iran AD - Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Y1 - 2018 PY - 2018 VL - 19 IS - 4 SP - 520 EP - 527 KW - MiR KW - 145 KW - Reactive Oxygen Species DO - 10.22074/cellj.2018.4550 N2 - ObjectiveReactive oxygen species (ROS) is an apoptosis inducer in pancreatic β-cells that stimulates p53/p65 mediated microRNA (miR)-145 expression. Punica granatum L. (pomegranate) is an antioxidant fruit that attenuates ROS generation. This study examines the effects of pomegranate fruit aqueous extract (PGE) on the levels of ROS, p53, p65, miR-145, and its target insulin receptor substrate 1 (irs-1) mRNA in Alloxan-diabetic male Wistar rats. Materials and Methods In this experimental study, diabetic rats received different doses of PGE. The effects of the PGE polyphenols were examined through a long-term PGE treatment period model, followed by an evaluation of the plasma and tissue contents of free fatty acids (FFAs), triglycerides (TG), and glycogen compared with diabetic controls (DC)and normal controls (NC). We used real-time polymerase chain reaction (PCR) to investigate the modulation of p53, p65, miR-145, and irs-1 expression levels. Results There was a noticeable reduction in fasting blood glucose (FBG) and ROS generation compared to DC. We observed marked decreases in p53, p65, miR-145 expression levels followed by an elevated level of irs-1, which contributed to improvement in insulin sensitivity. Conclusion PGE administration downregulated miR-145 levels in Alloxan-diabetic Wistar rats by suppression of ROS-mediated p53 and p65 overexpression. UR - https://www.celljournal.org/article_250459.html L1 - https://www.celljournal.org/article_250459_418b5e0cdc695eeef018f92fdae77c78.pdf ER -