Abstract
To investigate the effect of puerarin on insulin resistance and inflammation in rats with gestational diabetes mellitus (GDM). Gestational diabetic model rats were established by intraperitoneal injection of streptozotocin (25 mg/kg) combined with high-fat feeding and were randomly assigned to three groups: the control group, the GDM group, and the puerarin-treated group. Puerarin was intragastrically administered to rats daily until the offspring were born. The rats in both the GDM group and control group were administered the same volume of normal saline. Serum total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol in all groups of rats were measured. Haematoxylin and eosin staining was used to evaluate morphological changes in the liver, pancreas, and adipose tissues around the reproductive organs. Western blotting was carried out to measure the protein expression of IRS-1 and inflammatory factors, including TNF-α, TLR4, MyD88 and phosphorylated NF-κB, in the adipose tissues around the reproductive organs. Puerarin had preventive effects on GDM-induced pathological changes and ameliorated glucose and lipid metabolism disorders in GDM rats. Puerarin upregulated IRS-1 expression and decreased the protein expression of TNF-α, TLR4, and MyD88 as well as the levels of phosphorylated NF-κB in adipose tissues around the reproductive organs in GDM rats. This study indicated that puerarin exerts anti-inflammatory effects by downregulating the important TLR4/MyD88/NF-κB inflammatory signalling pathway. Therefore, puerarin can decrease the expression of TNF-α and ameliorate insulin resistance in GDM rats, suggesting the potential efficacy of puerarin in GDM treatment.
Highlights
Gestational diabetes mellitus (GDM) refers to hyperglycaemia in pregnant women with no prior history of diabetes mellitus
We found increased protein expression of toll-like receptor 4 (TLR4) and excessive inflammatory cytokines in the GDM rat model compared with control animals
To determine the role of the TLR4/Myeloid differentiation primary response gene 88 (MyD88)/nuclear factor-κB (NF-κB) pathway in puerarin-mediated inhibition of the inflammatory response, we studied the activities of TLR4, MyD88, p-NF-κB, and TNF-α in adipose tissues around the reproductive organs in GDM rats by western blotting to elucidate the precise molecular mechanism of the antiinflammatory activity of puerarin
Summary
Gestational diabetes mellitus (GDM) refers to hyperglycaemia in pregnant women with no prior history of diabetes mellitus. It is generally believed that GDM is associated with insulin resistance (IR) and high risks to the health of the mother and infant, including high blood pressure, foetal abnormalities, weight problems, and type II diabetes. These findings emphasize the need to optimize therapeutic approaches for GDM to maintain the health of mothers and offspring. Accumulating evidence suggests that chronic inflammation in GDM patients may cause abnormal regulation of insulin signalling and that inflammatory cytokines play important roles in the development of IR in GDM [5]. We found increased protein expression of TLR4 and excessive inflammatory cytokines in the GDM rat model compared with control animals
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