Identification of therapeutic effect of glucagon-like peptide 1 in the treatment of STZ-induced diabetes mellitus in rats by restoring the balance of intestinal flora.

OBJECTIVE: The objective of this study was to identify the therapeutic effect and the underlying mechanism of glucagon-like peptide 1 (GLP-1) in the treatment of STZ-induced diabetes mellitus (DM). METHODS: Mice were treated with STZ to establish an animal model of DM, which was further treated with a GLP-1 receptor agonist. Subsequently, the status of glucose, insulin, nitric oxide, inflammatory and oxidative factors was evaluated and compared among Sham, STZ, and STZ + GLP-1 groups. In addition, the intestinal flora spectrum in each group was also evaluated. RESULTS: In this study, it was found that the administration of STZ increased the level of glucose and glycosylated hemoglobin but reduced the level of insulin. It was also found that the levels of inflammation and oxidative stress in STZ-induced DM were both enhanced, as evidenced by a decreased level of catalase, superoxide dismutase, glutathione peroxidase, as well as increased levels of malonyldialdehyde, interleukin-1ß (IL-1ß), and IL-6. Meanwhile, the expression of nitric oxide, a factor associated with both oxidative stress and inflammation, was also suppressed in STZ-induced DM. More importantly, the imbalance of intestinal flora was observed in STZ-induced DM, as shown by a decreased level of both total bacteria and that of some strains including Clostridium, Bacteroides, Lactobacilli, and Bifidobacteria. CONCLUSION: In summary, the findings of this study confirmed the antihyperglycemic effect of GLP-1 and demonstrated that the therapeutic effect of GLP-1 in the treatment of STZ-induced DM was mediated, at least partially, by its ability to restore the balance of intestinal flora.

The Effects of Lentinan on the Expression Patterns of ß-Catenin, Bcl-2, and Bax in Murine Bone Marrow Cells Are Associated with Enhancing Dectin-1.

This study was focused on investigating the effect of lentinan (LNT) on the expression patterns of ß-catenin, Bcl-2, and Bax in murine bone marrow cells (BMCs). Adult BALB/L mice were divided into four groups (n = 10 for each group) that consisted of normal control adult BALB/L mice (control group) and adult BALB/L mice with intraperitoneal injection of low, medium, and high doses of LNT (LLen, MLen, and HLen, respectively). Cells of bone marrow from adult BALB/L mice were cultured in DMEM medium with or without laminarin (inhibitor of dectin-1) to investigate the role of dectin-1 in the effect of lentinan on the expression profile of ß-catenin, Bcl-2, and Bax using western blotting and RT-PCR methods. The ELISA results indicated that the expression profiles of dectin-1 were significantly elevated in BMCs from groups of LLen, MLen, and HLen compared with the control group (P < 0.05). The protein and gene expression profiles of ß-catenin and Bax increased significantly in murine BMCs from groups of MLen and HLen compared with the control group or the LLen group (P < 0.05). In contrast, the protein and gene expression levels of Bcl-2 decreased significantly in BMCs from the LLen, MLen, and HLen groups compared with the control group (P < 0.05). Furthermore, the expression profiles of ß-catenin, Bcl-2, and Bax reversed with the administration of laminarin (P < 0.05). Taken together, our results identified that the changing expression profiles of ß-catenin, Bcl-2, and Bax in murine BMCs are associated with enhancing dectin-1.

Disordered oropharyngeal microbial communities in H7N9 patients with or without secondary bacterial lung infection.

Secondary bacterial lung infection (SBLI) is a serious complication in patients with H7N9 virus infection, and increases disease severity. The oropharyngeal (OP) microbiome helps prevent colonisation of respiratory pathogens. We aimed to investigate the OP microbiome of H7N9 patients with/without secondary bacterial pneumonia using 16S rRNA gene sequencing. OP swab samples were collected from 51 H7N9 patients (21 with SBLI and 30 without) and 30 matched healthy controls (HCs) and used for comparative composition, diversity and richness analyses of microbial communities. Principal coordinates analysis successfully distinguished between the OP microbiomes of H7N9 patients and healthy subjects, and the OP microbiome diversity of patients with SBLI was significantly increased. There was significant dysbiosis of the OP microbiome in H7N9 patients, with an abundance of Leptotrichia, Oribacterium, Streptococcus, Atopobium, Eubacterium, Solobacterium and Rothia species in patients with SBLI, and Filifactor, Megasphaera and Leptotrichia species in patients without SBLI, when compared with HCs. Importantly, Haemophilus and Bacteroides species were enriched in HCs. These findings revealed dysbiosis of the OP microbiota in H7N9 patients, and identified OP microbial risk indicators of SBLI, suggesting that the OP microbiome could provide novel and non-invasive diagnostic biomarkers for early microbiota-targeted prophylactic therapies for SBLI prevention.