To investigate the regulatory effect of equol (Eq) on the susceptibility to metabolic syndrome (MS) in the offspring of rats with gestational diabetes mellitus (GDM).

Twenty female SD rats were divided into two groups: the normal group, which was fed a normal diet, and the GDM group, which was fed a high-fat diet (HFD) combined with intraperitoneal injection of streptozotocin. Each female rat was caged with a male to establish a normal pregnancy group and a GDM pregnancy group. The male offspring from the normal pregnancy group were randomly divided into two subgroups: blank control and MS model control. The male offspring from the GDM pregnancy group were randomly divided into five subgroups: MS model, low-, medium- and high-dose Eq (intragastric administration of 20, 40 and 80 mg/kg of Eq, respectively) and positive control (5 mg/kg of simvastatin). The blank control group was fed a normal diet, and the other groups were fed a HFD, with 8 rats in each group. The serum glucose and lipid metabolism indexes, oxidative stress and inflammation levels of GDM offspring rats were detected by commercial kits, and the degree of liver steatosis was observed by hematoxylin-eosin (HE) staining.

Compared with the MS group, Eq reduced the Lee’s index, final body mass and liver index of GDM offspring rats, and high-dose Eq decreased the Lee’s index by 13.9% (P < 0.01). Meanwhile, high-dose Eq significantly reduced serum triglyceride (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels (P < 0.05), highly significantly increased serum high-density lipoprotein cholesterol (HDL-C) levels (P < 0.01), and significantly reduced serum fasting blood glucose (FBG) and fasting insulin (FINS) levels (P < 0.05). Furthermore, it highly significantly lowered serum malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) levels and increased serum glutathione peroxidase (GSH-Px) levels (P < 0.01).

GDM offspring are more susceptible to MS than the offspring of normal pregnant rats. Eq can significantly improve abnormal glucose and lipid metabolism in GDM offspring, enhance antioxidant capacity, alleviate inflammation, and reduce MS in multiple ways.

To explore the effect of genistein (GEN) on relieving fatigue in immunosuppressed rats and the underlying mechanism.

A total of 96 male SD rats were randomly divided into six groups with 16 rats in each group, including blank control (CG), immunosuppression model (MG), low-dose GEN (LG), medium-dose GEN (MG), high-dose GEN (HG) and positive control (PG). All rats except those in the blank control group were injected intraperitoneally with cyclophosphamide at a dose of 40 mg/kg m_b for three days to establish an immunosuppressed rat model. The rats in the LG, MG and HG groups were gavaged with GEN at doses of 10, 20, and 40 mg/kg m_b, respectively. The positive control group was gavaged with 3.125 g/kg m_b of Zhenqi Fuzheng granule, and the blank control group was gavaged with an equal amount of peanut oil. After the experiment, the exhaustive swimming time of rats was recorded. The activities of creatine kinase (CK) and lactate dehydrogenase (LDH) in rat serum were detected by colorimetry. The concentrations of immunoglobulin G (IgG) and tumor necrosis factor-α (TNF-α) in rat serum were detected by enzymelinked immunosorbent assay (ELISA). Real-time fluorescence quantitative PCR was used to detect adenylate-activated protein kinase (AMPK), silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptorγ coactivator-1α (PGC-1α) and peroxisome proliferators-activated receptor-γ (PPARγ) mRNA expression levels. The protein expression levels of AMPK, SIRT1, PGC-1α and PPARγ in the skeletal muscle of rats were detected by Western blot.

Compared with the MG group, GEN supplementation significantly prolonged the exhaustive swimming time of rats (P < 0.01), and high-dose GEN significantly decreased CK and LDH activities and increased the concentrations of IgG and TNF-α in the serum (P < 0.01), and significantly increased the gene and protein expression levels of AMPK, SIRT1, PGC-1α and PPARγ in the skeletal muscle of rats (P < 0.05 and P < 0.01).

GEN relieves fatigue in immunosuppressed rats, and the underlying mechanism may be related to activating the AMPK/SIRT1/PGC-1α signaling pathway in the skeletal muscle and improving the exercise endurance, energy production and immunomodulatory capacity of rats.