Bingyun Li

Harbin Medical University, Charbin, Heilongjiang Sheng, China

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Publications (4)8.51 Total impact

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    ABSTRACT: Cross-sectional analysis was conducted to access the relationships between developing carotid artery atherosclerosis through consuming high fluoride in drinking water and its possible mechanism, using the baseline data collected from 585 study subjects. In the cross sectional analysis, subjects were divided into four groups based on the concentrations of fluoride in their drinking water. The range of fluoride concentrations was: normal group (less than 1.20mg/L), mild group (1.21-2.00mg/L), moderate group (2.01-3.00mg/L), and high concentration group (more than 3.01mg/L). The prevalence rate of carotid artery atherosclerosis in the subjects in each group was found to be 16.13%, 27.22%, 27.10%, and 29.69%, respectively. Significant difference between the prevalence of carotid artery atherosclerosis in the mild, moderate and high fluoride exposure group and in the normal group was observed (P<0.05). In addition, it was found that elevated intercellular cell adhesion molecule-1 (ICAM-1) and reduced glutathione peroxidases (GPx) was associated with carotid artery atherosclerosis in fluoride endemic areas. The findings of the research study revealed a significant positive relationship between excess fluoride exposure from drinking water and prevalence of carotid artery atherosclerosis in adults living in fluoride endemic areas. The possible mechanism was the excess fluoride induced the decreasing level of GPx causing the systemic inflammation and endothelial activation by oxidative stress.
    International journal of hygiene and environmental health 08/2013; · 2.64 Impact Factor
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    ABSTRACT: In this study, the relationships between high water fluoride exposure and essential hypertension as well as plasma ET-1 levels were investigated. A total of 487 residents aged 40 to 75 were randomly recruited from eight villages in Zhaozhou County from Heilongjiang Province in China and were divided into 4 groups according to the concentrations of fluoride in their water. Consumption levels of drinking water fluoride for normal, mild, moderate, and high exposure groups were 0.84±0.26mg/L, 1.55±0.22mg/L, 2.49±0.30mg/L, and 4.06±1.15mg/L, respectively. The prevalence of hypertension in each group was 20.16%, 24.54%, 32.30%, and 49.23%, respectively. There were significant differences between all the groups; namely, with the increase in water fluoride concentrations, the risk of essential hypertension in adults grows in a concentration-dependent manner. Significant differences were observed in the plasma ET-1 levels between the different groups (P<0.0001). In the multivariable logistic regression model, high water fluoride concentrations (F(-)≥3.01mg/L, OR(4/1)=2.84), age (OR(3/1)=2.63), and BMI (OR(2/1)=2.40, OR(3/1)=6.03) were closely associated with essential hypertension. In other words, the study not only confirmed the relationship between excess fluoride intake and essential hypertension in adults, but it also demonstrated that high levels of fluoride exposure in drinking water could increase plasma ET-1 levels in subjects living in fluoride endemic areas.
    Science of The Total Environment 12/2012; 443C:864-869. · 3.16 Impact Factor
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    ABSTRACT: Over the past two decades, fluoride effects on osteoclasts have been evaluated; however, its molecular mechanisms remain unclear. In this study, we investigated the effect of fluoride on osteoclast formation, function, and regulation using osteoclasts formed from mice bone marrow macrophages treated with the receptor activator of NF-κB ligand and macrophage colony-stimulating factor. Our data showed that fluoride levels ≤ 8 mg/L had no effect on osteoclast formation; however, it significantly reduced osteoclast resorption at 0.5 mg/L. Fluoride activity on bone resorption occurred through the inhibition of nuclear factor of active T cells (NFAT) c1 expression. Furthermore, the expression of its downstream genes, including the dendritic cell-specific transmembrane protein, c-Src, the d2 isoform of vacuolar (H+) ATPase v0 domain, matrix metalloproteinase 9, and cathepsin K were decreased, leading to impaired osteoclast acidification, reduced secretion of proteolytic enzymes, and decreased bone resorption. In summary, our results suggested that fluoride has different roles in osteoclast formation and function. Fluoride ≤ 8 mg/L did not impact osteoclast formation; however, it significantly decreased the resorption activity of newly formed osteoclasts. The molecular mechanism of fluoride action may involve inhibition of NFATc1 and its downstream genes. © 2012 Wiley Periodicals, Inc. Environ Toxicol, 2012.
    Environmental Toxicology 05/2012; · 2.71 Impact Factor
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    ABSTRACT: : Receptor activator of nuclear factor kappa-B ligand (RANKL) acting on osteoblasts is an essential cytokine for osteoclast formation. Recent studies have shown that fluoride (F) can stimulate RANKL expression of osteoblasts. However, the effect of F under various levels of RANKL on osteoclast formation is not clear. In this study, stem cell technology was used to observe the effect of F on osteoclast formation at different levels of treatment with RANKL. Our results show that F significantly inhibits the formation of osteoclasts treated with 50 ng/mL RANKL. The number of osteoclasts in the 0.5 mg/L F group fell to about 60% of the control group with no further significant change at the higher fluoride concentrations used (2 and 8 mg/L). On the other hand, F had no effect on the formation of osteoclasts treated with 100 ng/mL RANKL. In fact, the number of osteoclasts formed at 100 ng/mL RANKL was significantly higher than at the 50 ng/mL RANKL level. However, F significantly decreased the activity of osteoclast bone resorption even at a low level of 0.5 mg/L F, and the higher the F concentration was, the lower the activity of bone resorption became. Therefore we conclude that the main effect of F on osteoclasts was the inhibition of their capacity for bone resorption, thus resulting in osteosclerosis as the major clinical manifestation in patients with skeletal fluorosis. Keywords: Bone resorption; Fluoride effect on osteoblasts; Fluoride effect on osteoclasts; Osteoclast formation; RANKL (Receptor activator of nuclear factor kappa-B ligand). INTRODUCTION Skeletal fluorosis, the most serious consequence of fluorosis, is a bone disease with osteosclerosis as the major clinical outcome, mostly involving bone joints, causing ligament calcifications, accompanied in various degrees by osteopenia, osteoporosis and osteomalacia. 1,2 The diversity of clinical manifestations of skeletal fluorosis is associated with the complexity of bone metabolism. The process of bone metabolism includes bone resorption by osteoclasts and bone formation by osteoblasts. A tight interplay between these two kinds of cells is essential to maintain homeostasis of bone. 3 One study found that osteoblasts, while active, secrete more cytokines such as receptor activator of nuclear factor kappa-B ligand (RANKL), which can stimulate formation of osteoclasts, thereby increasing bone resorption and maintaining homeostasis of bone metabolism. 4 Furthermore, osteoblasts treated with a low dose of F show enhanced proliferation with increase in bone formation. 5,6 Moreover, recent studies indicate that F can stimulate the RANKL expression of osteoblasts. 7,8 However, the effect of F under various levels of RANKL on osteoclast formation as part of bone resorption remains unknown. In order to provide some profiles for further clarifying the pathogenesis of skeletal fluorosis, stem cell technology was used in the present study to observe the effect of F on osteoclast formation by treatment with different levels of RANKL.