​Protective effect of tectorigenin​ against streptozotocin-induced gestational diabetes mellitus in rats via alteration of inflammation, oxidative stress, HO-1/Nrf2 and NF-κB/COX-2/iNOS signaling pathway.

Gestational diabetes mellitus (GDM) is a prevalent metabolic disorder during pregnancy, characterized by hyperglycemia and associated with significant maternal and fetal complications. The current study was investigating the protective effect of tectorigenin against streptozotocin (STZ)-induced GDM in rats. STZ was used for the induction of diabetes in the rats and pregnant rats that received the oral administration of tectorigenin and blood glucose level were estimated at different time intervals (day 3, day 12, and day 18). The foetus weight, placental weight and placental index, plasma insulin level, HOMA-IR, HOMA-β, HOMA-ISI, food intake, water intake, urine output, fecal output, hepatic glycogen, free fatty acid, serum C-peptide, antioxidant, inflammatory cytokines and inflammatory parameters were estimated. The different mRNA expressions were also estimated. Tectorigenin treatment significantly suppressed the blood glucose level and improved the insulin level. Tectorigenin treatment significantly altered the body weight, foetus weight, placental weight, placental index, water intake, food intake, urine output, fecal output, fasting insulin level, HOMA-IR, HOMA-β, HOMA-ISI, hepatic glycogen, serum C-peptide, free fatty acid and visfatin. Tectorigenin treatment significantly (P < 0.001) altered the level of lipid parameters (VLDL, TC, TG, HDL, LDL); antioxidant parameters (GPx, SOD, TAC, LPO, CAT, GSH); inflammatory cytokines (TGF-β, TNF-α, IL-1β, IL-6, IL-10, MCP-1); inflammatory parameters (NF-κB, COX-2, iNOS); ICAM-1, VCAM-1, HO-1 and Nrf2. Tectorigenin treatment significantly altered the mRNA expression of COX-2, iNOS, NF-κB, TLR4, MyD88 and NLRP3. Tectorigenin exerts a protective effect against STZ-induced GDM ion rats via alteration of HO-1/Nrf2 and NF-κB/COX-2/iNOS signaling.