Melatonin Attenuates AlCl 3 -Induced Apoptosis and Osteoblastic Differentiation Suppression by Inhibiting Oxidative Stress in MC3T3-E1 Cells

Aluminum (Al) inhibits osteoblast-mediated bone formation by oxidative stress, resulting in Al-induced bone disease. Melatonin (MT) has received extensive attention due to its antioxidant and maintenance of bone health effect. To evaluate the protective effect and mechanism of MT on AlCl -induced os...

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Bibliographic Details
Published inBiological trace element research Vol. 196; no. 1; p. 214
Main Authors Cao, Zheng, Geng, Xue, Jiang, Xinpeng, Gao, Xiang, Liu, Kexiang, Li, Yanfei
Format Journal Article
LanguageEnglish
Published United States 01.07.2020
Subjects
3T3 Cells
Aluminum Chloride - antagonists & inhibitors
Aluminum Chloride - pharmacology
Animals
Apoptosis - drug effects
Cell Differentiation - drug effects
Cell Survival - drug effects
Melatonin - pharmacology
Mice
Osteoblasts - drug effects
Oxidative Stress - drug effects
Osteoblastic differentiation
Oxidative stress
Melatonin
Aluminum chloride
Apoptosis
p53
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Summary:Aluminum (Al) inhibits osteoblast-mediated bone formation by oxidative stress, resulting in Al-induced bone disease. Melatonin (MT) has received extensive attention due to its antioxidant and maintenance of bone health effect. To evaluate the protective effect and mechanism of MT on AlCl -induced osteoblast dysfunction, MC3T3-E1 cells were treated with MT (100 μM) and/or AlCl (8 μM). First, MT alleviated AlCl -induced osteoblast dysfunction, presenting as the reduced apoptosis rate as well as increased cell viability, alkaline phosphatase (ALP) activity, and type I collagen (COL-1) level. Then, MT significantly attenuated AlCl -induced oxidative stress, presenting as the reduced reactive oxygen species and 8-hydroxy-2'-deoxyguanosine levels as well as increased glutathione level and superoxide dismutase activity. Finally, MT protected MC3T3-E1 cells against p53-dependent apoptosis and differentiation suppression, as assessed by Caspase-3 activity, protein levels of p53, Bcl-2-associated X protein (Bax), B cell lymphoma gene 2 (Bcl-2), cytosolic Cytochrome c, Runt-related transcription factor 2 (Runx2), and Osterix, as well as the mRNA levels of Bax, Bcl-2, Runx2, Osterix, ALP, and COL-1. Overall, our findings demonstrate MT attenuates AlCl -induced apoptosis and osteoblastic differentiation suppression by inhibiting oxidative stress in MC3T3-E1 cells.
ISSN:1559-0720