The association between dietary intake of flavonoids and its subclasses and the risk of metabolic syndrome

BackgroundThe healthiest way to prevent metabolic syndrome (MetS) is through behavioral and nutritional adjustments. We examined the relationship between total flavonoids intake, flavonoid subclasses, and clinically manifest MetS.MethodsA cross-sectional analysis was conducted among 28,719 individuals from the National Health and Nutrition Examination Survey (NHANES) and Food and Nutrient Database for Dietary Studies (FNDDS) 2007–2011 and 2017–2018. Two 24-h reviews were conducted to determine flavonoids intake and subclasses. The link between flavonoids intake and MetS was investigated using a multivariate logistic regression model.ResultsQ2 and Q3 of total flavonoids intake were associated with 20 and 19% lower risk of incident MetS after adjusting age and sex. Anthocyanidins and flavanones intake in Q2 and Q3 substantially reduced the MetS risk compared to Q1. MetS risk decreased steadily as the total intake of flavonoids increased to 237.67 mg/d. Flavanones and anthocyanidins also displayed V-shaped relationship curves (34.37 and 23.13 mg/d).ConclusionMetS was adversely linked with total flavonoids intake, flavanones, and anthocyanidins. Moreover, the most effective doses of total flavonoids, flavanones, and anthocyanidins were 237.67, 34.37, and 23.13 mg/d, respectively, potentially preventing MetS

DNA damage response(DDR): a link between cellular senescence and human cytomegalovirus

Abstract The DNA damage response (DDR) is a signaling cascade that is triggered by DNA damage, involving the halting of cell cycle progression and repair. It is a key event leading to senescence, which is characterized by irreversible cell cycle arrest and the senescence-associated secretory phenotype (SASP) that includes the expression of inflammatory cytokines. Human cytomegalovirus (HCMV) is a ubiquitous pathogen that plays an important role in the senescence process. It has been established that DDR is necessary for HCMV to replicate effectively. This paper reviews the relationship between DDR, cellular senescence, and HCMV, providing new sights for virus-induced senescence (VIS)

DZNep inhibits the proliferation of colon cancer HCT116 cells by inducing senescence and apoptosis

AbstractEZH2 is over-expressed in human colon cancer and is closely associated with tumor proliferation, metastasis and poor prognosis. Targeting and inhibiting EZH2 may be an effective therapeutic strategy for colon cancer. 3-Deazaneplanocin A (DZNep), as an EZH2 inhibitor, can suppress cancer cell growth. However, the anti-cancer role of DZNep in colon cancer cells has been rarely studied. In this study, we demonstrate that DZNep can inhibit the growth and survival of colon cancer HCT116 cells by inducing cellular senescence and apoptosis. The study provides a novel view of anti-cancer mechanisms of DZNep in human colon cancer cells

Sulfated glucuronomannan hexamer inhibits lipid accumulation and ameliorates atherosclerosis in apolipoprotein E-deficient mice

Atherosclerosis (AS) is the leading cause of cardiovascular diseases worldwide, which generates huge health and economic burdens on humanity. The anti-atherosclerosis activities of glucuronomannan oligosaccharides (Gs) and sulphated glucuronomannan oligosaccharides (SGs) were investigated in vitro and in vivo. Among these Gs and SGs, G6S1 (higher sulphated glucuronomannan hexamer) decreased the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), then down-regulated NF-κB signaling pathway to reduce the release of TNF-α and IL-1β, and targeted PI3K/Akt/mTOR signaling pathway to enhance autophagy in a dose-dependent manner, which showed the best anti-atherosclerosis activity. Moreover, data showed that G6S1 improves liver function, reduced the progression and promoted the stabilization of atherosclerotic plaques, and also decreases LOX-1 expression in plaque macrophages in ApoE-/- mice. In summary, our data indicated that sulfated glucuronomannan hexamer exhibited the anti-atherosclerosis through down-regulating LOX-1 in macrophages, and the degree of polymerization and sulphation had essential roles in anti-atherosclerosis bioactivity of oligosaccharides

Dietary flavonoids intake contributes to delay biological aging process: analysis from NHANES dataset

Abstract Background Diet may influence biological aging and the discrepancy (∆age) between a subject’s biological age (BA) and chronological age (CA). We aimed to investigate the correlation of dietary flavonoids with the ∆age of organs (heart, kidney, liver) and the whole body. Method A total of 3193 United States adults were extracted from the National Health and Nutrition Examination Survey (NHANES) in 2007–2008 and 2017–2018. Dietary flavonoids intake was assessed using 24-h dietary recall method. Multiple linear regression analysis was performed to evaluate the association of dietary flavonoids intake with the ∆age of organs (heart, kidney, liver) and the whole body. BA was computed based on circulating biomarkers, and the resulting ∆age was tested as an outcome in linear regression analysis. Results The ∆age of the whole body, heart, and liver was inversely associated with higher flavonoids intake (the whole body ∆age β = − 0.58, cardiovascular ∆age β = − 0.96, liver ∆age β = − 3.19) after adjustment for variables. However, higher flavonoids intake positively related to renal ∆age (β = 0.40) in participants with chronic kidney disease (CKD). Associations were influenced by population characteristics, such as age, health behavior, or chronic diseases. Anthocyanidins, isoflavones and flavones had the strongest inverse associations between the whole body ∆age and cardiovascular ∆age among all the flavonoids subclasses. Conclusion Flavonoids intake positively contributes to delaying the biological aging process, especially in the heart, and liver organ, which may be beneficial for reducing the long-term risk of cardiovascular or liver disease

Association between lncRNA GAS5, MEG3, and PCAT-1 Polymorphisms and Cancer Risk: A Meta-Analysis

Purpose. Long noncoding RNAs (lncRNAs) have been widely studied, and single nucleotide polymorphisms (SNPs) in lncRNAs are considered to be genetic factors that influence cancer susceptibility. The lncRNA GAS5, MEG3, and PCAT-1 polymorphisms are shown to be possibly associated with cancer risk. The aim of this meta-analysis was to systematically evaluate this association. Methods. Studies were selected from PubMed, Web of Science, Embase, Google Scholar, Cochrane Library, the Chinese National Knowledge Infrastructure (CNKI), and the Chinese Biomedical Literature Database (CBM) through inclusion and exclusion criteria. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using the random-effects model or fixed-effects model to assess the association between lncRNA polymorphisms and cancer susceptibility. Metaregression and publication bias analyses were also conducted. All analyses were performed using the Stata 12.0 software. Results. Sixteen articles (covering 13750 cases and 17194 controls) were included in this meta-analysis. A significant association between SNP rs145204276 and gastric cancer risk was observed (del vs. ins: OR=0.79, 95%CI=0.72‐0.86; del/del vs. ins/ins+del/ins: OR=0.74, 95%CI=0.59‐0.91; del/ins vs. ins/ins: OR=0.84, 95%CI=0.67‐1.05). For rs16901904, a decreased cancer risk was observed in three genetic models (C vs. T: OR=0.79, 95%CI=0.70‐0.90; CC vs. CT+TT: OR=0.49, 95%CI=0.37‐0.65; CC vs. TT: OR=0.49, 95%CI=0.37‐0.66). No statistical significance was found in the metaregression analysis. For all of the included SNPs, no publication bias was found in all genotype models. Conclusions. The rs145204276 SNP in lncRNA GAS5 is likely to be associated with gastric cancer risk, whereas the rs16901904 SNP in lncRNA PCAT-1 bears association with a decreased cancer risk

RAW data of "senescence sensitize cells to 50 Hz MFs"

Raw images and files of the data presented in the manuscript and supplementary information

RhoA promotes osteoclastogenesis and regulates bone remodeling through mTOR-NFATc1 signaling

Abstract Background The cytoskeletal architecture of osteoclasts (OCs) and bone resorption activity must be appropriately controlled for proper bone remodeling, which is associated with osteoporosis. The RhoA protein of GTPase plays a regulatory role in cytoskeletal components and contributes to osteoclast adhesion, podosome positioning, and differentiation. Although osteoclast investigations have traditionally been performed by in vitro analysis, however, the results have been inconsistent, and the significance of RhoA in bone physiology and pathology is still unknown. Methods We generated RhoA knockout mice by specifically deleting RhoA in the osteoclast lineage to understand more about RhoA’s involvement in bone remodeling. The function of RhoA in osteoclast differentiation and bone resorption and the mechanisms were assessed using bone marrow macrophages (BMMs) in vitro. The ovariectomized (OVX) mouse model was adopted to examine the pathological effect of RhoA in bone loss. Results Conditional deletion of RhoA in the osteoclast lineage causes a severe osteopetrosis phenotype, which is attributable to a bone resorption suppression. Further mechanistic studies suggest that RhoA deficiency suppresses Akt-mTOR-NFATc1 signaling during osteoclast differentiation. Additionally, RhoA activation is consistently related to the significant enhancement the osteoclast activity, which culminates in the development of an osteoporotic bone phenotype. Furthermore, in mice, the absence of RhoA in osteoclast precursors prevented occurring OVX-induced bone loss. Conclusion RhoA promoted osteoclast development via the Akt-mTOR-NFATc1 signaling pathway, resulting a osteoporosis phenotype, and that manipulating RhoA activity might be a therapeutic strategy for osteoporotic bone loss