Key Laboratory of Etiology and Epidemiology

Harbin, China

Key Laboratory of Etiology and Epidemiology

Harbin, China
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Li B.-Y.,Harbin Medical University | Li B.-Y.,Key Laboratory of Etiology and Epidemiology | Gao Y.-H.,Harbin Medical University | Gao Y.-H.,Key Laboratory of Etiology and Epidemiology | And 8 more authors.
International Journal of Molecular Medicine | Year: 2017

Epidemiological investigations indicate that certain ingredients in tea bricks can antagonize the adverse effects of fluoride. Tea polyphenols (TPs), the most bioactive ingredient in tea bricks, have been demonstrated to be potent bone-supporting agents. ClC 7 is known to be crucial for osteoclast (OC) bone resorption. Thus, in this study, we investigated the potential protective effects of TPs against fluorosis using a mouse model and explored the underlying mechanisms with particular focus on ClC 7. A total of 40, healthy, 3 week old male C57BL/6 mice were randomly divided into 4 groups (n=10/group) by weight as follows: distilled water (control group), 100 mg/l fluoridated water (F group), water containing 10 g/l TPs (TP group) and water containing 100 mg/l fluoride and 10 g/l TPs (F + TP group). After 15 weeks, and after the mice were sacrificed, the long bones were removed and bone marrow-derived macrophages were cultured ex vivo in order to perform several experiments. OCs were identified and counted by tartrate resistant acid phosphatase (TRAP) staining. The consumption of fluoride resulted in severe fluorosis and in an impaired OC function [impaired bone resorption, and a low mRNA expression of nuclear factor of activated T-cells 1 (NFATc1), ATPase H+ transporting V0 subunit D2 (ATP6v0d2) and osteopetrosis associated transmembrane protein 1 (Ostm1)]. In the F + TP group, fluorosis was attenuated and OC function was restored, but not the high bone fluoride content. Compared with the F group, mature OCs in the F + TP group expressed higher mRNA levels of ClC 7 and Ostm1; the transportation and retaining of Cl was improved, as shown by the fluorescence intensity experiment. On the whole, our findings indicate that TPs mitigate fluorosis in C57BL/6 mice by regulating OC bone resorption. Fluoride inhibits OC resorption by inhibiting ClC 7 and Ostm1, whereas TPs attenuate this inhibitory effect of fluoride.

Sun L.,Harbin Medical University | Sun L.,Key Laboratory of Etiology and Epidemiology | Gao Y.,Harbin Medical University | Gao Y.,Key Laboratory of Etiology and Epidemiology | And 6 more authors.
Environmental Toxicology and Pharmacology | Year: 2014

The purpose of this study was to explore the effects of high fluoride and high fat on triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), total antioxidant capacity (T-AOC), lipid peroxide (LPO) and malondialdehyde (MDA) in rabbits. A factorial experimental design was used, with two factors (fluoride and fat) and three levels. Seventy-two male rabbits were randomly assigned into nine groups according to initial weight and serum lipid levels. The rabbits were fed with basic feed, moderate fat feed or high fat feed and drank tap water, fluoridated water at levels of 50 and 100. mg. fluorion/L freely. Biological materials were collected after 5 months, and serum lipid, T-AOC, LPO, and MDA levels were then measured. Using these data, the separate and interactive effects of high fluoride and high fat were analyzed. High fluoride and high fat both increased serum levels of TC, HDL-C and LDL-C significantly (. P< 0.05), and there was also a synergistic effect between high fluoride and high fat (. P< 0.05). High fluoride and high fat had different effects on TG levels: high fat significantly increased TG levels (. P< 0.01) whereas high fluoride had nothing to do with TG levels (. P> 0.05). High fat significantly elevated LPO and MDA levels and lowered T-AOC levels in serum (. P< 0.05). Similarly, high fluoride significantly increased LPO and MDA levels in serum (. P< 0.05). However, there was no interactive effect between high fat and high fluoride on these indexes. In summary, high fluoride and high fat increased serum TC and LDL-C levels individually and synergistically, and this would cause and aggravate hypercholesterolemia in rabbits. At the same time, high fluoride and high fat both made the accumulation of product of oxidative stress in experimental animals. © 2014 Elsevier B.V.

Wang C.,Harbin Medical University | Wang C.,Key Laboratory of Etiology and Epidemiology | Gao Y.,Harbin Medical University | Gao Y.,Key Laboratory of Etiology and Epidemiology | And 14 more authors.
BMJ Open | Year: 2012

Objective: To assess the effects of provided fluoridesafe drinking-water for the prevention and control of endemic fluorosis in China. Design: A national cross-sectional study in China. Setting: In 1985, randomly selected villages in 27 provinces (or cities and municipalities) in 5 geographic areas all over China. Participants: Involved 81 786 children aged from 8 to 12 and 594 698 adults aged over 16. Main outcome measure: The prevalence of dental fluorosis and clinical skeletal fluorosis, the fluoride concentrations in the drinking-water in study villages and in the urine of subjects. Results: The study showed that in the villages where the drinking-water fluoride concentrations were higher than the government standard of 1.2 mg/l, but no fluoride-safe drinking-water supply scheme was provided (FNB areas), the prevalence rate and index of dental fluorosis in children, and prevalence rate of clinical skeletal fluorosis in adults were all significantly higher than those in the historical endemic fluorosis villages after the fluoride-safe drinking-water were provided (FSB areas). Additionally, the prevalence rate of dental fluorosis as well as clinical skeletal fluorosis, and the concentration of fluoride in urine were found increased with the increase of fluoride concentration in drinking-water, with significant positive correlations in the FNB areas. While, the prevalence rate of dental fluorosis and clinical skeletal fluorosis in different age groups and their degrees of prevalence were significantly lower in the FSB areas than those in the FNB areas. Conclusions: The provision of fluoride-safe drinkingwater supply schemes had significant effects on the prevention and control of dental fluorosis and skeletal fluorosis. The study also indicated that the dental and skeletal fluorosis is still prevailing in the high-fluoride drinking-water areas in China.

Sun L.,Harbin Medical University | Gao Y.,Harbin Medical University | Liu H.,Harbin Medical University | Zhang W.,Harbin Medical University | And 5 more authors.
Science of the Total Environment | Year: 2013

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, OR4/1=2.84), age (OR3/1=2.63), and BMI (OR2/1=2.40, OR3/1=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. © 2012 Elsevier B.V.

Ma X.,Harbin Medical University | Han S.,Harbin Medical University | Zhang W.,Harbin Medical University | Zhang W.,Key Laboratory of Etiology and Epidemiology | And 4 more authors.
Molecular Medicine Reports | Year: 2015

Previous studies have suggested that hepatocyte apoptosis may be a fundamental underlying mechanism of liver injury and diseases, such as liver fibrosis. Relaxin3 has been reported to have antifibrotic actions in the heart and to attenuate isoproterenolinduced myocardial injury; however, the beneficial role of relaxin3 on hepatocyte apoptosis remains to be elucidated. The aim of the present study was to explore the role and possible mechanisms of relaxin3 through hydrogen peroxide (H2O2)induced apoptosis in primary human hepatocytes. Cells were treated with relaxin3 and then cell viability, morphological features, the presence of cleaved caspases as well as the levels of endoplasmic reticulum stress (ERS) protein markers and autophagy markers were evaluated. The H2O2 group showed significantly decreased cell viability, increased apoptosis as well as upregulation of caspases (cleaved caspase3, 8 and 9) and ERS protein markers compared with those of the control group. However, cells treated with relaxin3 (10 ng/ml) demonstrated improved cell viability, reduced apoptosis and decreased expression of cleaved caspases and ERS markers. However, the expression of autophagy markers remained unchanged following H2O2induced apoptosis and relaxin3 treatment. In conclusion, relaxin3 was shown to protect hepatocytes from H2O2induced apoptosis via downregulation of cleaved caspase8 and 9, as well as inhibition of the ERS pathway.

Zhu D.,Harbin Medical University | Zhang L.,Harbin Medical University | Cheng L.,Harbin Medical University | Ren L.,Harbin Medical University | And 3 more authors.
Kidney and Blood Pressure Research | Year: 2016

Background/Aims: We aimed to evaluate whether pancreatic kininogenase (PKase) can relieve renal fibrosis and investigate its mechanisms in diabetic nephropathy (DN) rats Methods: We established streptozotocin (STZ) induced-DN rats. After treatment with PKase for 4 weeks, urinary weight, urinary protein content and blood glucose concentration were detected, and then renal histopathological changes were examined using Hematoxylin and Eosin (H&E) and Masson's thrchrome staining. In addition, the expressions of miR-433, transforming growth factor-β1 (TGF-β1) and antizyme inhibitor 1 (Azin1) were detected by qRT-PCR and/or western blotting. Results: PKase reduced urinary weight, urinary protein contents and blood glucose concentrations. PKase treated DN rats exhibited less renal fibrosis than untreated DN rats (P < 0.05). Furthermore, the expression levels of TGF-β and miR-433 were reduced (P < 0.05), while Azin1 expression was increased in renal tissues of PKase treated DN rats compared with untreated DN rats (P < 0.05). Conclusions: PKase might not only inhibit the development of DN by reducing urinary weight, urinary protein content and blood glucose concentration in DN rats, but also relieve renal fibrosis in DN rats through inhibiting the expression of TGF-β1, and miR-433 and Azin1 might involve in this process. © 2016 The Author(s).

Yu J.,Harbin Medical University | Liu P.,Harbin Medical University | Liu Y.,Harbin Medical University | Liu S.J.,Harbin Medical University | And 2 more authors.
BMJ Open | Year: 2014

Objective: To contribute evidence relevant to the policy of supplying iodised salt (IS), non-iodised salt (NIS) or both in Chinese cities. Design: Subnational telephone interview survey. Setting: China. Participants: Totally, 24 557 telephone numbers were dialled and 4833 citizens accepted the telephone interview. The telephone numbers were randomly selected by random digit dialling and a Mitofsky-Waksberg two-stage sampling method in 17 capital cities and 6 coastal cities from 17 iodine deficiency disorder (IDD)-eliminated provinces (municipalities). Results: The 4833 citizens finished the telephone interview. Among them, 3738 (77.3%) citizens chose IS, 481 (10%) citizens chose NIS, and the others chose both IS and NIS. The citizens' awareness rates of IDD and IDD preventive measures were 68.7% and 62.5%, respectively. Conclusions: It is not a suitable time to supply IS and NIS simultaneously in the developed cities of China, but a pilot project may be conducted in the cities where IDD has been sustainably eliminated, there is strong awareness of IDD and the population can make informed decisions regarding IS. IDD health education should be further strengthened, especially regarding the potential for IQ damage.

Yu J.,Harbin Medical University | Yu J.,Key Laboratory of Etiology and Epidemiology | Gao Y.,Harbin Medical University | Gao Y.,Key Laboratory of Etiology and Epidemiology | And 2 more authors.
Biological Trace Element Research | Year: 2013

The ratio of osteoprotegerin ligand (OPGL) to osteoprotegerin (OPG) determines the delicate balance between bone resorption and synthesis. The main objective of the present study is to investigate the possible role of OPGL and OPG in the bone metabolism of rats exposed to fluoride and the protective or aggravating effect of calcium (Ca). In a 6-month study, 270 weanling male Sprague-Dawley rats weighing between 70 and 90 g were divided randomly into six groups of 45 rats in each group. Three groups (groups I, III, and V)served as controls and drank deionized water and were fed purified rodent diets containing either 1,000 mg Ca/kg (low Ca), 5,000 mg Ca/kg (normal Ca), or 20,000 mg Ca/kg (high Ca). The three experimental groups (groups II, IV, and VI) were given the same diets but they drank water containing 100 mg F ion/L (from NaF). Every 2 months 15 rats were randomly selected from each group and sacrificed for the study. The ratio of OPGL mRNA to OPG mRNA was significantly increased by the sixth month in the distal femur joints of the F-exposed rats. Serum tartrate-resistant acid phosphatase activity and serum calcitonin activity in the F-exposed groups was increased, although changes were not apparent in the serum alkaline phosphatase or Gla-containing proteins, especially in the low calcium and high calcium diet F-exposed groups. The results indicated that OPG and OPGL may play important roles in skeletal fluorosis, and that fluoride may enhance osteoclast formation and induce osteoclastic bone destruction. A high Ca diet did not play a protective role, but rather may aggravate the damage of fluoride. © 2013 Springer Science+Business Media New York.

Zhang W.,Harbin Medical University | Zhang W.,Key Laboratory of Etiology and Epidemiology | Feng H.,Harbin Medical University | Feng H.,Key Laboratory of Etiology and Epidemiology | And 19 more authors.
Biological Trace Element Research | Year: 2013

Although studies have shown that arsenic exposure can induce apoptosis in a variety of cells, the exact molecular mechanism of chronic arsenicosis remains unclear. Based on our previous study on human serum, the present study was to determine whether pigment epithelium-derived factor (PEDF) plays a role in the damage induced by chronic arsenic exposure in a rat model and to explore the possible signaling pathway involved. Thirty male Wistar rats were randomly divided into three groups and the arsenite doses administered were 0, 10, and 50 mg/L, respectively. The experiment lasted for 6 months. Our results showed that level of arsenic increased significantly in serum, liver, brain, and kidney in arsenic-exposed groups. It was indicated that PEDF protein was widely distributed in the cytoplasm of various types of cells in liver, brain, and kidney. PEDF protein level was only changed when the arsenite dose reached 50 mg/L in liver and brain, whereas it was not changed in the kidney. In order to investigate the possible mechanism of PEDF-exerted damages upon arsenite exposure, apoptosis in liver and brain was assessed. The proportion of apoptotic cells gradually increased with increasing arsenic administration. The ratio of Bax/Bcl-2 in the high arsenic group (50 mg/L) was significantly higher than that in the control group. Therefore, we thought PEDF played a role in cell apoptosis of liver and brain which induced by sodium arsenite exposure, and the results also demonstrated that Bax and Bcl-2 might be two key targets in the action of PEDF. © 2012 Springer Science+Business Media New York.

Liu H.,Harbin Medical University | Liu H.,Key Laboratory of Etiology and Epidemiology | Gao Y.,Harbin Medical University | Gao Y.,Key Laboratory of Etiology and Epidemiology | And 8 more authors.
International Journal of Hygiene and Environmental Health | Year: 2014

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 1.20. mg/L), mild group (1.21-2.00. mg/L), moderate group (2.01-3.00. mg/L), and high concentration group (more than 3.01. mg/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. © 2013 Elsevier GmbH.

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