ABSTRACT
OBJECTIVE: We aimed to investigate the effect of Lycium barbarum polysaccharide (LBP) on the proliferation and differentiation of osteoblasts in postmenopausal individuals with osteoporosis using in vitro cell experiments. METHODS: We assessed the effect of long-term LBP consumption on the intestinal metabolites of individuals using a simulation of the human intestinal microbiota ecosystem. We also tested the capacity of LBP in proliferating MC3T3-E1 cells using the cell counting kit-8 (CCK-8) method and analyzed the effect of intestinal metabolites on the osteogenic differentiation of MC3T3-E1 cells by testing bone metabolism viability with relevant indicators. RESULTS: The level of short-chain fatty acids (SCFAs) significantly increased (p < 0.05), and the concentrations of acetic acid, propionic acid, and butyric acid all showed an upward trend after the treatment using LBP. At appropriate concentrations, the fermentation supernatant can enhance osteoblast proliferation by significantly increasing the active expression of bone-alkaline phosphatase (B-ALP) and osteocalcin (OCN) in osteoblasts (p < 0.05). CONCLUSION: By modulating the metabolites of intestinal microbiota, production of SCFAs, the prebiotic properties of LBP can enhance osteoblast differentiation through in vitro simulation experiment and cell-based assay.
ABSTRACT
Although recent evidence has revealed that a body shape index (ABSI) is correlated with the incidence of death among different ethnicities, there remains a paucity of studies investigating the impact of ABSI on mortality within the Chinese elderly. Our objective was to ascertain the link between ABSI, as well as its alterations over time, and all-cause mortality among Chinese aged 65 y and above. A total of 3789 participants were enrolled from the Chinese Longitudinal Healthy Longevity Survey (CLHLS). Cox regressions and restricted cubic splines were employed to assess the association of ABSI and relative changes with all-cause mortality. When nonlinearity was detected, a restricted cubic spline regression was subsequently conducted to compute hazard ratios and 95% confidence intervals. The median survival time was 46 months, and 1342 individuals (35.4%) were reported to have died. ABSI contributed independently to rising death rates among Chinese old populations according to univariate and multivariate Cox regressions. Statistically significant associations were also found stratified by age, sex, and lifestyle. A U-shaped association of ABSI changes with all-cause mortality (p = 0.027) was observed, indicating that old adults with stable ABSI during the follow-up period experienced the lowest risk of mortality. After multivariable adjustment, participants with a 10% reduction in ABSI changes had an increased 9.4% risk of death, while participants with a 10% rise in ABSI changes had an increased 1.9% risk. ABSI and its changes are predictors for all-cause mortality among the elderly Chinese population, which emphasizes the clinical importance of monitoring ABSI and keeping it stable over time.
Subject(s)
East Asian People , Mortality , Somatotypes , Aged , Humans , Anthropometry , Retrospective Studies , Risk Factors , Waist CircumferenceABSTRACT
Background LINC00665 is a newly identified oncogene, which has been reported to be oncogene in various cancers. Nevertheless, its role in the progression of colorectal cancer (CRC) remains obscure to the extent. This study aimed at exploring the role and mechanism of LINC00665 in CRC progression. Materials and methods RNA and protein expression were detected via qRT-PCR and western blot. Functional assays were conducted to investigate the role of LINC00665 in the CRC cellular processes. TOP/FOP assay was performed to detect the activity of Wnt/ß-catenin signaling pathway. Mechanism investigations were carried out to explore the regulatory relationship among genes. Results LINC00665 was overtly expressed in CRC cell lines at high levels. Functionally, silencing of LINC00665 could curb in vitro CRC cell growth, migration and invasion, while stimulating cell apoptosis. Mechanically, LINC00665 sponged miR-214-3p to up-regulate CTNNB1 expression, consequently activating Wnt/ß-catenin signaling pathway. Furthermore, LINC00665 could bind to U2AF2 and enhance the association between U2AF2 and CTNNB1, increasing the stability of CTNNB1. CTNNB1 overexpression could reverse the suppressive effects of LINC00665 downregulation. Conclusion LINC00665 stimulates CRC progression through the activation of Wnt/ß-catenin signaling pathway, which hopefully might be a therapeutic target for CRC.
