Objective To evaluate the efficacy of Huangqi-Sijunzi decoction combined with conventional western medicine in treatment of gestational diabetes mellitus(GDM). Methods A total of 103 patients with GDM who met the inclusion criteria were randomly divided into control group and treatment group (52 in each group).The control group was treated with GDM standardized treatment, and the treatment group was addedHuangqi-Sijunzi decoction on the basis of the control group. Both groups were treated for 14 days. The ELISA was used to detect serum CRP and adiponectin, and Mg2+ was detected by automatic biochemical analyzer. Pregnancy outcome observed and recorded, and the adverse reaction was recorded. Results After the treatment, the levels of FPG, 2 hPG and HbAlc in the treatment group were significantly lower than those in the control group (t=7.352,17.962, 9.713, P<0.01); and the level of CRP in the treatment group was significantly lower than that in the control group. While the Mg2+ and adiponectin were significantly higher than those in the control group (t=9.275, 4.206,6.021, P<0.01). After the treatment, the incidence of abortion, fetal macrosomia, cesarean section and polyhydramnios in the treatment group were significantly lower than that in the control group (χ2=5.358, 7.262, 3.992, 6.116, P<0.05).Conclusions The Huangqi-Sijunzi decoction combined with conventional western medicine can improve the blood sugar level of GDM patients, reduce the incidence of adverse pregnancy outcomes, and improve the clinical efficacy.

Background: Long non-coding RNAs (lncRNAs) have been illustrated to contribute to the development of gestational diabetes mellitus (GDM). In the present study, we aimed to elucidate how lncRNA taurine upregulated gene 1 (TUG1) influences insulin resistance (IR) in a high-fat diet (HFD)-induced mouse model of GDM. Methods: We initially developed a mouse model of HFD-induced GDM, from which islet tissues were collected for RNA and protein extraction. Interactions among lncRNA TUG1/microRNA (miR)-328-3p/sterol regulatory element binding protein 2 (SREBP-2) were assessed by dual-luciferase reporter assay. Fasting blood glucose (FBG), fasting insulin (FINS), homeostasis model assessment of insulin resistance (HOMA-IR), HOMA pancreatic β-cell function (HOMA-β), insulin sensitivity index for oral glucose tolerance tests (ISOGTT) and insulinogenic index (IGI) levels in mouse serum were measured through conducting gain- and loss-of-function experiments. Results: Abundant expression of miR-328 and deficient expression of lncRNA TUG1 and SREBP-2 were characterized in the islet tissues of mice with HFD-induced GDM. LncRNA TUG1 competitively bound to miR-328-3p, which specifically targeted SREBP-2. Either depletion of miR-328-3p or restoration of lncRNA TUG1 and SREBP-2 reduced the FBG, FINS, HOMA-β, and HOMA-IR levels while increasing ISOGTT and IGI levels, promoting the expression of the extracellular signal-regulated kinase (ERK) signaling pathway-related genes, and inhibiting apoptosis of islet cells in GDM mice. Upregulation miR-328-3p reversed the alleviative effects of SREBP-2 and lncRNA TUG1 on IR. Conclusion Our study provides evidence that the lncRNA TUG1 may prevent IR following GDM through competitively binding to miR-328-3p and promoting the SREBP-2-mediated ERK signaling pathway inactivation.