miR-27b-3p Improved High Glucose-Induced Spermatogenic Cell Damage via Regulating Gfpt1/HBP Signaling

<b><i>Introduction:</i></b> Diabetes mellitus (DM)-induced testicular damage is characterized by abnormal apoptosis of spermatogenic cells. Here, we clarified the roles and the molecular mechanism of microRNA (miR)-27b-3p in high glucose (HG)-induced spermatogenic cell damage. <b><i>Methods:</i></b> GC-1 spg cells were treated with 30 mmol/L glucose for 24 h. Cell viability was assessed by 2.3 3-(4, 5-dimethylthiazolyl2)-2, 5-diphenyltetrazolium bromide (MTT) assay. And, levels of O-linked N-acetylglucosamine (OGT), apoptosis-related proteins, and autophagy-related proteins were evaluated using Western blot. Levels of tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and UDP-N-acetylglucosamine (UDP-GlcNAc) were assessed by enzyme linked immunosorbent (ELISA) assay. Levels of reactive oxygen species (ROS), malonic dialdehyde (MDA) and activity of superoxide dismutase (SOD) in cells were determined using kits. Cell apoptosis was determined using flow cytometry assay. Besides, dual luciferase reporter assay was employed to verify the binding relationship between miR-27b-3p and glutamine-fructose-6-phosphate transaminase 1 (Gfpt1). <b><i>Results:</i></b> miR-27b-3p was markedly downregulated in HG-treated GC-1 spg cells. HG treatment caused decreased cell viability, increased oxidative stress and inflammation, and induced autophagy and apoptosis, which were abolished by miR-27b-3p overexpression. miR-27b-3p suppressed the activation of hexosamine biosynthetic pathway (HBP) signaling in HG-treated spermatogenic cells. miR-27b-3p directly bound to Gfpt1 and negatively regulated its expression. <b><i>Conclusion:</i></b> miR-27b-3p could improve HG-induced spermatogenic cell damage via regulating Gfpt1/HBP signaling, providing a new treatment strategy for the treatment of DM-induced testicular damage.

POTENSI KANDUNGAN ANTIOKSIDAN RUMPUT KEBAR (Biophytum Petersianum Klotzsch) TERHADAP APOPTOSIS DAN GAMBARAN HISTOPATOLOGIS TESTIS PADA MENCIT (MUS MUSCULUS) YANG DIPAPAR 2,3,7,8-Tetrachlorodibenzo-p-dioxin

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most toxic compound in the dioxin group. This compound is a pollutant for the environment and very harmful to human health and enter the body through the mucous membranes in the mouth and the respiratory tract and can be transmitted through the placenta and lactation. The aim of this study was to know the antioxidantpotency of to resolve reproduction disturbance caused by TCDD exposure.Thirty Balb/C male mice were divided into five different groups, the negative control group, a positive control group exposed to TCDD at a dose of 7 μg/kg BW, P1 group of groups exposed to TCDD doses of 7 μg / kg BW and given Biophytum petersianum extract 0.05mg/gBB/day, group P2 group exposed to TCDD doses of 7μg/kgBW and given 0.080mg/gBB/day, and group P3 were exposed to TCDD dose of 7μg/kgBB and given the extract of Biophytum petersianum 0.135mg/gBB/day during day 2 to day 55. On the 56th day the mice were sacrificed and apoptotic examination and spermatogenic cell histopathological features were performed on the testis. The results showed that: P2 (0,433 ± 0,497; p<0,05) and P3 (0,200 ± 0,000 p<0,05) groups were the most effective group in decreasing spermatogenic cell apoptosis compared to positive control group (2,933 ± 1,5832 p<0,05). The Johnsen score result showed that P2 (9,400 ± 0,420) and P3 (9,800 ± 0,253) groups improving the histopathologic picture of spermatogenic cells in seminiferous tubules compared to positive control group (7,20 ± 0,400) p<0,05. Conclusion of this study were Biophytum petersianum is effective to solve reproduction disturbances caused by exposure of TCDD and the P3 group is the most effective group.