Polysaccharides from wild morels alter gut microbiota, increase the production of SCFAs and promote the proliferation of lymphocytes in mice.
The study evaluates efficacy and safety of recombinant human parathyroid hormone (1–34) [rhPTH (1–34)] and alendronate (ALN) in the treatment of postmenopausal osteoporosis. Totally 65 postmenopausal women with osteoporosis were divided into 2 groups. PTH group received daily subcutaneous injection of rhPTH (1–34), and ALN group were treated orally with ALN per week. Bone mineral density (BMD) of lumbar spine (1–4), femoral neck, and total hip, serum levels of calcium, phosphorus, total cholesterol, triglyceride, alkaline phosphatase (ALP), N-terminal propeptide of type I collagen (PINP), and C-telopeptide of type I collagen (CTX) were tested before treatment and at week 24 and 48 after treatment. Serum levels of vascular endothelial growth factor (VEGF) and platelet-derived growth factor-BB (PDGF-BB) were measured before treatment and at week 48 after treatment. The rhPTH (1–34) increased BMD of lumbar spine (1–4), but decreased BMD of femoral neck and total hip at week 48 after treatment. By contrast, ALN enhanced BMD of lumbar spine (1–4) and femoral neck, but reduced BMD of total hip at week 48 after treatment. In PTH group, serum levels of PINP, ALP, and β-CTX were significantly elevated above baseline at week 24 and 48 after treatment. Treatment with ALN decreased levels of PINP, ALP, and β-CTX compared with baseline at week 24 and 48 after treatment. rhPTH (1–34) and ALN significantly decreased levels of PDGF-BB, but not levels of VEGF. rhPTH (1–34) increased levels of calcium, phosphorus and triglyceride, but decreased levels of total cholesterol. ALN increased levels of calcium and triglyceride, but reduced levels of phosphorus and total cholesterol. rhPTH (1–34) and ALN were safe in the treatment of postmenopausal osteoporosis. The study demonstrates that efficacy of rhPTH (1–34) on BMD of lumbar spine (1–4) is similar to that of alendronate in the treatment of postmenopausal osteoporosis. The effect of rhPTH (1–34) on BMD of femoral neck or total hip is weaker than that of ALN. In addition, rhPTH (1–34) increases BMD of lumbar spine (1–4) maybe by raising serum levels of VEGF, but reduces BMD of femoral neck and total hip maybe by decreasing serum levels of PDGF-BB.
Polysaccharides from morels possess many characteristics beneficial to health, such as anti-tumor and immunomodulatory activities. The gut microbiota plays a critical role in the modulation of immune function. However, the impact of morel polysaccharides on the gut microbiota has not yet been explored. In this study, a high-throughput pyrosequencing technique was used to investigate the effects of MP, a new heteropolysaccharide extracted from wild morels, on the diversity and composition of microbiota along the intestine in mice, as well as the production of short-chain fatty acids (SCFAs). The results showed that MP treatment increased the number of operational taxonomic unit (OTUs) and diversity along the intestine, especially in the small intestine. MP treatment induced a significant decrease in the number of Firmicutes and a significant increase in the number of Bacteroidetes in the small intestine microbiota. It was also observed that the relative abundance of SCFA-producing bacteria, especially Lachnospiraceae , was increased in both the cecum and colon of MP-treated mice. Moreover, MP promoted the production of SCFAs in mice. These results provide a foundation for further understanding the health benefits conferred by morel polysaccharides.
Targeting cyclin-dependent kinases (CDKs) is a promising method of therapy for cancer. Unfortunately, the efficacy of CDK inhibitors in hepatocellular carcinoma (HCC) is limited, due in part to incomplete understanding of cell cycle progression and a lack of specific biomarkers to adequately identify which patients may be responsive to CDK inhibitors. In the present study, we report that microtubuleassociated protein RP/EB family member 1 (MAPRE1), a gene involved in cell cycle and microtubule regulation, is significantly increased in HCC tissue, promotes HCC cell proliferation, enhances in vitro tumorigenesis, and associates with poor prognosis of HCC. We demonstrate that MAPRE1 binds with CDK2, resulting in the hyperphosphorylation of the CDK2 Thr161 residue in HCC cells. Our findings reveal that targeting MAPRE1 might be an effective therapeutic strategy in HCC, and suggest that MAPRE1 expression might provide a promising biomarker to stratify patients with HCC who may benefit from treatment with CDK inhibitors.
AIM: To discuss the effects and mechanism of microRNA-34a in cell apoptosis induced by osteoarthritis. METHODS: Collection of the normal and osteoarthritis synovial tissues and measurements of the miRNA-34a and TGIF2 gene expression. In the cell experiment, the cells were divided into Control, Blank and miRNA inhibitor group. The cell proliferation and apoptosis of the different groups were measured by MTT and fl ow cytometry and the TGIF2 protein expression in the different groups was evaluated by WB assay. The correlation between TGIF2 and miRNA-34a was analyzed by Double luciferase experiment. RESULTS: Compared with normal synovial tissues, the miRNA-34a gene expression was signifi cantly up-regulated and TGIF2 gene expression was signifi cantly suppressed in osteoarthritis synovial tissues (p < 0.001, respectively). The cell proliferation was signifi cantly depressed and the cell apoptosis rate was signifi cantly increased in miRNA inhibitor group compared with the Control group (p < 0.001, respectively). Using the WB assay it was shown that the TGIF2 protein expression of miRNA inhibitor group was signifi cantly suppressed compared with that of Control group (p < 0.01). By Double luciferase assay, TGIF2 gene was one target gene of miRNA-34a. CONCLUSION: miRNA-34a could induce osteoarthritis synovial cell apoptosis via regulation of TGIF2 in vitro (Fig. 6, Ref. 29). Text in PDF www.elis.sk.
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