Melatonin Attenuates AlCl3-Induced Apoptosis and Osteoblastic Differentiation Suppression by Inhibiting Oxidative Stress in MC3T3-E1 Cells
Melatonin Attenuates AlCl3-Induced Apoptosis and Osteoblastic Differentiation Suppression by Inhibiting Oxidative Stress in MC3T3-E1 Cells
复制标题
褪黑激素通过抑制 MC3T3-E1 细胞的氧化应激来减轻 AlCl3 诱导的细胞凋亡和成骨细胞分化抑制
DOI：
10.1007/s12011-019-01893-2
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发表时间：
2020-07-01
影响因子：
3.9
通讯作者：
Li, Yanfei
中科院分区：
文献类型：
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作者：
Cao, Zheng;Geng, Xue;Li, Yanfei
铝(Al)通过氧化应激抑制成骨细胞介导的骨形成，导致铝诱导的骨病。褪黑素(MT)因其抗氧化和维持骨骼健康的作用而受到广泛关注。为探讨MT对AlCl3诱导的成骨细胞功能障碍的保护作用及其机制，用MT(100μM)和/或AlCl3(8μM)处理MC3T3-E1细胞。首先，MT减轻了AlCl3诱导的成骨细胞功能障碍，表现为细胞凋亡率降低，细胞存活率、碱性磷酸酶(ALP)活性和I型胶原(Col-1)水平升高。MT显著减轻了AlCl3诱导的氧化应激，表现为减少了活性氧和8-羟基-2‘-脱氧鸟苷水平，增加了谷胱甘肽水平和超氧化物歧化酶活性。最后，MT通过Caspase-3活性、P53、Bcl2相关X蛋白(Bax)、B细胞淋巴瘤基因2(Bcl2)、胞浆细胞色素c、Runx2和Osterix的蛋白水平以及Bax、Bcl2、Runx2、Osterix的mRNA水平来评估MT对MC3T3-E1细胞的保护作用。总体而言，我们的研究结果表明，MT通过抑制氧化应激来减轻AlCl3诱导的MC3T3-E1细胞的凋亡和成骨细胞分化抑制。
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.