Corn baked by burning coal triggered overexpression of osteopontin in hepatocytes of rats following fluorosis

Zhou, Yueming; Mo, Sui-Lin; Wang, Rui Hua; Liu, Weifeng; Ji-chan, Liu; Wang, Jiaqi; He, Jiang; Zhang, Hua; Guan, Zhi‐Zhong; Zhou, Shu‐Feng; Yu, Yu

doi:10.1177/0748233711410905

Cited by 9 publications

(3 citation statements)

References 14 publications

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“…Endemic fluorosis, including brick tea‐type, water borne, and coal‐burning fluorosis, is a chronic systemic cumulative poisoning caused by a long term excessive intake of fluoride in drinking water, food, and air 3,4 . So far, endemic fluorosis remains a concern for global public health, particularly, the area severely affected by coal‐burning endemic fluorosis was Guizhou province, China 5 . Endemic fluorosis is a chronic systemic malady, characterized by dental and skeletal fluorosis 6 .…”

Section: Introductionmentioning

confidence: 99%

miR‐486‐3p regulates CyclinD1 and promotes fluoride‐induced osteoblast proliferation and activation

Ouyang

Yu²,

Luo

et al. 2021

Environmental Toxicology

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Fluoride is a persistent environmental pollutant, and its excessive intake contributes to skeletal and dental fluorosis. The mechanisms underlying fluoride‐induced abnormal osteoblast proliferation and activation, which are related to skeletal fluorosis, have not yet been fully clarified. As important epigenetic regulators, microRNAs (miRNAs) participate in bone metabolism. On the basis of our previous miRNA‐seq results and bioinformatics analysis, this study investigated the role and specific molecular mechanism of miR‐486‐3p in fluoride‐induced osteoblast proliferation and activation via CyclinD1. Herein, in the fluoride‐challenged population, we observed that miR‐486‐3p expression decreased while CyclinD1 and transforming growth factor (TGF)‐β1 increased, and miR‐486‐3p level correlated negatively with the expression of CyclinD1 and TGF‐β1 genes. Further, we verified that sodium fluoride (NaF) decreases miR‐486‐3p expression in human osteoblasts and overexpression of miR‐486‐3p reduces fluoride‐induced osteoblast proliferation and activation. Meanwhile, we demonstrated that miR‐486‐3p regulates NaF‐induced upregulation of CyclinD1 by directly targeting its 3′‐untranslated region (3′‐UTR). In addition, we observed that NaF activates the TGF‐β1/Smad2/3/CyclinD1 axis and miR‐486‐3p mediates transcriptional regulation of CyclinD1 by TGF‐β1/Smad2/3 signaling pathway via targeting TGF‐β1 3′‐UTR in vitro. This study, thus, contributes significantly in revealing the mechanism of miR‐486‐3p‐mediated CyclinD1 upregulation in skeletal fluorosis and sheds new light on endemic fluorosis treatment.

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Section: Introductionmentioning

confidence: 99%

miR‐486‐3p regulates CyclinD1 and promotes fluoride‐induced osteoblast proliferation and activation

Ouyang

Yu²,

Luo

et al. 2021

Environmental Toxicology

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“…Nutrition may play an important role in the development of fluorosis. Studies have not been successful at establishing a consistent association between CBF risk and specific foods and nutrients [e.g., corn (5,6) chili (6), sour soup (7), vitamins (8)(9)(10)(11), and calcium (12,13)]. The inconsistent results linking foods and fluorosis may, in part, reflect the difficulty of disentangling the high degree of correlation among dietary constituents.…”

Section: Introductionmentioning

confidence: 99%

Association Between Dietary Patterns and Fluorosis in Guizhou, China

et al. 2020

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Objective: Many studies have explored the effects of individual foods or nutrients on fluorosis, but no studies have focused on dietary patterns. This study examined the relationship between dietary patterns and coal-burning fluorosis in Guizhou, China. Methods: This 1:1 matched case-control study was conducted in Zhijin County of Guizhou province with a sample size of 200 cases of fluorosis and 200 age and gender matched controls. Habitual dietary intake was assessed by face-to-face interviews, using a validated 75-item food frequency questionnaire (FFQ) and various covariates using structured questionnaires. The dietary patterns were identified by factor analysis. Results: The factor analysis identified three major dietary patterns which were labeled healthy, easy-to-roast and high protein. After adjusting for various confounding factors, a decreased risk for fluorosis was observed in the highest tertile of the healthy dietary pattern relative to the lowest tertile (OR = 0.47, 95% CI = 0.27-0.84, P-trend = 0.003) and a positive association was observed between the easy-to-roast dietary pattern and fluorosis risk (OR = 2.05, 95% CI = 1.15-3.66), with a significant linear trend (P = 0.017). We did not find an association between fluorosis risk and the high protein dietary pattern. The relationships remained significant when the analyses were stratified by gender and fluorosis subtypes. Conclusion: The healthy dietary pattern may lower coal-burning fluorosis risk; in contrast, the easy-to-roast dietary pattern significantly increases the risk of coalburning fluorosis.

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“…Hepatitis refers to a group of diseases caused by a variety of pathogenic factors which damage the liver and induce inflammation [1]. As a result, hepatocytes are destroyed, and the liver function is impaired, further leading to symptoms.…”

Section: Introductionmentioning

confidence: 99%

Magnesium isoglycyrrhizinate protects against concanavalin A-induced immunological liver injury in a mouse model

Jiang

Zheng

2019

Revista Romana De Medicina De Laborator

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Background: To evaluate the protective effects of magnesium isoglycyrrhizinate on a mouse model of concanavalin A (ConA)-induced immunological liver injury. Materials and Methods: Forty-eight mice were randomly divided into a normal control group, a model group, three dose groups of magnesium isoglycyrrhizinate (12.5, 25, 50 mg/kg) and a dexamethasone group (2.5 mg/kg). Magnesium isoglycyrrhizinate was intraperitoneally injected for 5 consecutive days, and the model of immunological liver injury was established on the fifth day after caudal vein injection of ConA (20 mg/kg). Blood was collected to detect the activities of alanine transaminase (ALT) and aspartate transaminase (AST) as well as the levels of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). The levels of neopterin (NP) and malondialdehyde (MDA) and the activities of myeloperoxidase (MPO) and superoxide dismutase (SOD) in liver tissues were measured, and histopathological changes were observed. Results: The serum levels of ALT and AST in the model group increased. Hepatic lobules had necrotic foci and inflammatory cell infiltration. The plasma levels of TNF-α and IFN-γ increased. In liver tissues, the levels of NP, MDA and MPO rose, but that of SOD decreased. Magnesium isoglycyrrhizinate significantly attenuated the activities of ALT and AST (P<0.05). Histopathological staining showed that inflammation of the liver was relieved significantly. Magnesium isoglycyrrhizinate also decreased the levels of NP, MDA and MPO in liver tissues (P<0.05), raised that of SOD and reduced the plasma levels of TNF-α and IFN-γ (P<0.05). Conclusion: Magnesium isoglycyrrhizinate protected against ConA-induced immunological liver injury in mice, probably through immune regulation and antioxidation.

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Corn baked by burning coal triggered overexpression of osteopontin in hepatocytes of rats following fluorosis

Cited by 9 publications

References 14 publications

miR‐486‐3p regulates CyclinD1 and promotes fluoride‐induced osteoblast proliferation and activation

miR‐486‐3p regulates CyclinD1 and promotes fluoride‐induced osteoblast proliferation and activation

Association Between Dietary Patterns and Fluorosis in Guizhou, China

Magnesium isoglycyrrhizinate protects against concanavalin A-induced immunological liver injury in a mouse model

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