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https://www.selleckchem.com/products/itacitinib-incb39110.html Gestational diabetes mellitus (GDM) is one of the common complications of pregnant women, with serious threatening to pregnant women and newborns. The pathogenesis of GDM remains unclear now. This study aims to explore the effects of miR-22-3p targeted regulation of suppressors of cytokine signaling 3 (Socs3) on the hepatic insulin resistance (HIR) in mice with GDM. Healthy SPF C57BL/6J mice were selected to establish GDM model and divided into 7 groups Normal group, Model group, NC-(negative control) mimic group, miR-22-3p mimic group, NC-pcDNA3.0 group, pcDNA3.0-Socs3 group, and miR-22-3p mimic + pcDNA3.0-Socs3 group. The islet morphology, and the expressions of miR-22-3p, Socs3 mRNA and Socs3 protein in the islet tissues were detected by HE staining, qRT-PCR and Western blot. Fasting blood glucose (FBG), triglyceride (TG), total cholesterol (TC), and high-density lipoprotein cholesterol (HDL-C) were measured. Oral glucose tolerance test (OGTT) was performed to detect FBG and fasting insulin (FINS) contents, and insulin resistance (HOMA-IR) was calculated. Compared with the Normal group, the model group had decreased levels of miR-22-3p and HDL-C, while increased levels of Socs3 mRNA and protein expressions, OGTT, FBG, FINS, and HOMA-IR, TG and TC (all P < 0.05). Compared with the Model group, the above indicators (OGTT, FBG, FINS, HOMA-IR, TG, TC and HDL-C) were improved in the miR-22-3p mimic group, but worsened in the pcDNA3.0-Socs3 group (all P < 0.05). miR-22-3p can down-regulate the expression of Socs3, thereby inhibiting HIR in GDM mice. miR-22-3p can down-regulate the expression of Socs3, thereby inhibiting HIR in GDM mice.In animal models, hepatocytes can be reprogrammed into insulin-producing cells (IPCs) for a novel antidiabetic treatment. However, the potential for an immunologic reaction and issues with gene integration of the viral vehicle hamper system efficacy. Here, we adopted an Ultra

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