No abstract

The present study was designed to investigate the hypoglycemic effects of glabridin from licorice in an animal model of diabetes mellitus (DM). Male Kunming mice were used to induce DM using streptozotocin (STZ). After confirmation of the diabetic state, the mice were randomly divided into six groups of 10 animals each: normal control (NC), diabetic control (DC), diabetic + low-dose glabridin treatment (DLG) (glabridin, 10 mg/kg), diabetic + medium‑dose glabridin treatment (DMG) (glabridin, 20 mg/kg), diabetic + high-dose glabridin treatment (DHG) (glabridin, 40 mg/kg) and diabetic + glyburide treatment group (DG) (glyburide, 4 mg/kg). Each treatment was continued daily for 28 days, and then body weight, fasting blood glucose (FBG), glucose tolerance, superoxide dismutase (SOD) and malondialdehyde (MDA) were measured. The data obtained showed that glabridin significantly increased body weight, glucose tolerance and SOD activities in the liver, kidney and pancreas, while decreasing FBG levels and MDA content in the liver, kidney and pancreas. These results demonstrated that glabridin possesses hypoglycemic effects.

Transforming growth factor-β1 (TGF-β1) is critical in controlling inflammatory responses and the prevention of autoimmune diseases. Although the effect of TGF-β1 on macrophages from normal mice or rats has been established, little attention has been paid to its effect on disease conditions. In the present study, we investigated the regulatory effect, and possible mechanism, of TGF-β1 exposure on the secretion of nitric oxide (NO) in peritoneal macrophages (PMΦ) obtained from collagen-induced arthritis (CIA) rats. The CIA model was established by immunizing the emulsion of collagen type II and incomplete Freund's adjuvant (IFA) in Wistar rats. PMΦ were incubated with TGF-β1 (5 ng/ml) for 36 h and the supernatant, and cell mRNA and protein were collected. NO concentration was determined using an NO assay kit. The mRNA expression of inducible nitric oxide synthase (iNOS) and Toll-like receptor 4 (TLR4) was determined using reverse transcription-polymerase chain reaction (RT-PCR). The protein expression of iNOS was tested with western blot analysis. The expression of membrane TLR4 was determined by flow cytometry. We discovered that the secretion of NO from the PMΦ of CIA rats increased compared with normal rats. TGF-β1 significantly inhibited the production of NO in the PMΦ from CIA rats. iNOS mRNA and protein expression in the PMΦ from CIA rats may be suppressed by TGF-β1. TLR4 mRNA and protein expression in PMΦ from CIA rats were upregulated with LPS stimulation and treatment with TGF-β1 inhibited their expression. These results demonstrated that TGF-β1 inhibited lipopolysaccharide (LPS)-induced NO production in the PMΦ from CIA rats, which may be due to the inhibition of the LPS-TLR4 signaling pathway.

CD4+CD25+ regulatory T cells (CD4+CD25+ Tregs) have been shown to play a regulatory or suppressive role in the immune response and are possibly relevant to the pathogenesis of autoimmune diseases. In the present study, we attempted to investigate the frequency of CD4+CD25+ Tregs in peripheral blood (PB) of collagen-induced arthritis (CIA) rats during the development of arthritis, to determine whether their frequency is involved in the immunoregulation of this disease. The results showed that normal rats had similar frequencies of CD4+CD25+ Tregs in PB during the experiment time, expressed as a percentage of CD4+CD25+Foxp3+ T cells among the CD4+ T lymphocyte population. In contrast, the frequency of CD4+CD25+Foxp3+ T cells in CIA rats was found to change during the development of arthritis. In CIA rats, there is a significant negative correlation between the frequency of CD4+CD25+Foxp3+ T cells and paw swelling (r=-0.786, p< 0.01). The relationship between the frequency of CD4+CD25+Foxp3+ T and immune activation was not found in normal rats. During the time course, the frequency of CD4+CD25+Foxp3+ T was lower in CIA rats than in normal ones. The data suggest that the frequency of PB CD4+CD25+ Tregs may be a promising marker for arthritis activity.

No abstract

CD4+CD25+ regulatory T cells (CD4+CD25+ Tregs)have been shown to play a regulatory or suppressive role in the immune response and are possibly relevant to the pathogenesis of autoimmune diseases. In the present study, we attempted to investigate the frequency of CD4+CD25+ Tregs in peripheral blood (PB) of collagen-induced arthritis (CIA) rats during the development of arthritis, to determine whether their frequency is involved in the immunoregulation of this disease. The results showed that normal rats had similar frequencies of CD4+CD25+ Tregs in PB during the experiment time, expressed as a percentage of CD4+CD25+Foxp3+ T cells among the CD4+ T lymphocyte population. In contrast, the frequency of CD4+CD25+Foxp3+ T cells in CIA rats was found to change during the development of arthritis. In CIA rats, there is a significant negative correlation between the frequency of CD4+CD25+Foxp3+ T cells and paw swelling (r=− 0.786, p＜ 0.01). The relationship between the frequency of CD4+CD25+Foxp3+ T and immune activation was not found in normal rats. During the time course, the frequency of CD4+CD25+Foxp3+ T was lower in CIA rats than in normal ones. The data suggest that the frequency of PB CD4+CD25+ Tregs may be a promising marker for arthritis activity.