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MECHANISM OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR γ AGONISTS IMPROVING INSULIN RESISTANCE IN GESTATIONAL DIABETES

XUEYU YIN *

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This study examined how the Peroxisome Proliferator-Activated Receptor γ (PPARγ) agonists rosiglitazone and GW1929 influence insulin resistance and cellular hebavior in trophoblasts from gestational diabetes mellitus (GDM) with particular attention to the High Mobility Group Box 1 (HMGB1)/Nuclear Factor Kappa-B (NF-κB) pathway. Primary trophoblast cells were assigned to four groups: untreated controls, insulin resistance (IR) induced with 10 µmol/L insulin, and two IR groups additionally treated with 10 µmol/L rosiglitazone or GW1929. Proliferation, apoptosis, and HMGB1/NF-κB pathway activity were then compared across groups using standard statistical methods. Compared with controls, IR-treated cells showed lower glucose consumption and proliferation, higher apoptosis, and elevated HMGB1, NF-κB p65 (mRNA and protein), along with increased TNF-α, IL-6, IL-17, TLR4, hs-CRP, and GSK-3β (p < 0.05). Both rosiglitazone and GW1929 reversed these changes: glucose consumption and proliferation rose, apoptosis fell, and HMGB1, NF-κB p65, and the inflammatory markers listed above all decreased relative to the IR group (p < 0.05). Together, these findings indicate that PPARγ agonists can alleviate insulin resistance in GDM trophoblasts, support proliferation, and suppress apoptosis and inflammation, likely by dampening HMGB1/NF-κB pathway activation.