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Human Primary Trophoblast Cell Culture Model to Study the Protective Effects of Melatonin Against Hypoxia/reoxygenation-induced Disruption
Published on: July 30, 2016
Melatonin Attenuates AlCl3-Induced Apoptosis and Osteoblastic Differentiation Suppression by Inhibiting Oxidative
Zheng Cao1,2, Xue Geng1, Xinpeng Jiang3
1Northeastern Science Inspection Station, China Ministry of Agriculture Key Laboratory of Animal Pathogen Biology, College of Veterinary Medicine, Northeast Agricultural University, NO. 600 Changjiang Street, Xiangfang District, Harbin, 150030, China.
Abstract:
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 AlCl3-induced osteoblast dysfunction, MC3T3-E1 cells were treated with MT (100 μM) and/or AlCl3 (8 μM). First, MT alleviated AlCl3-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 AlCl3-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 AlCl3-induced apoptosis and osteoblastic differentiation suppression by inhibiting oxidative stress in MC3T3-E1 cells.
Insights
Melatonin (MT) protects bone cells from aluminum toxicity by reducing oxidative stress and apoptosis. This study shows MT preserves osteoblast function and differentiation, offering potential therapeutic benefits for aluminum-induced bone disease.
Area of Science:
- Biochemistry
- Cell Biology
- Toxicology
Background:
- Aluminum (Al) exposure causes bone disease by inducing oxidative stress and inhibiting osteoblast function.
- Melatonin (MT), a potent antioxidant, is investigated for its potential to counteract Al-induced bone damage.
Purpose of the Study:
- To investigate the protective effects and underlying mechanisms of Melatonin (MT) against Aluminum chloride (AlCl3)-induced dysfunction in MC3T3-E1 osteoblasts.
- To evaluate MT's ability to mitigate oxidative stress and apoptosis in osteoblasts exposed to AlCl3.
Main Methods:
- MC3T3-E1 cells were treated with varying concentrations of MT and AlCl3.
- Assessed cell viability, apoptosis rates, alkaline phosphatase (ALP) activity, and type I collagen (COL-1) levels.
- Measured reactive oxygen species (ROS), 8-hydroxy-2'-deoxyguanosine (8-OHdG), glutathione (GSH) levels, and superoxide dismutase (SOD) activity.
- Analyzed p53-dependent apoptosis markers (Caspase-3, p53, Bax, Bcl-2, Cytochrome c) and osteogenic differentiation markers (Runx2, Osterix, ALP, COL-1) at protein and mRNA levels.
Main Results:
- MT treatment significantly reduced AlCl3-induced osteoblast apoptosis and increased cell viability, ALP activity, and COL-1 levels.
- MT effectively attenuated AlCl3-induced oxidative stress by decreasing ROS and 8-OHdG levels, while increasing GSH levels and SOD activity.
- MT protected osteoblasts by inhibiting p53-dependent apoptosis and preserving the expression of key osteogenic differentiation factors.
Conclusions:
- Melatonin (MT) demonstrates a significant protective effect against Aluminum chloride (AlCl3)-induced osteoblast dysfunction.
- MT mitigates AlCl3 toxicity by inhibiting oxidative stress and suppressing p53-dependent apoptosis pathways.
- These findings suggest MT holds therapeutic potential for managing aluminum-induced bone diseases by preserving osteoblast health and function.
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