| 2 | Melatonin protects TEGDMA-induced preodontoblast mitochondrial apoptosis via the JNK/MAPK signaling pathway显示文摘Resin monomer-induced dental pulp injury presents a pathology related to mitochondrial dysfunction.Melatonin has been regarded as a strong mitochondrial protective bioactive compound from the pineal gland.However,it remains unknown whether melatonin can prevent dental pulp from resin monomer-induced injury.The aim of this study is to investigate the effects of melatonin on apoptosis of mouse preodontoblast cells(mDPC6T)induced by triethylene glycol dimethacrylate(TEGDMA),a major component in dental resin,and to determine whether the JNK/MAPK signaling pathway mediates the protective effect of melatonin.A well-established TEGDMA-induced mDPC6T apoptosis model is adopted to investigate the preventive function of melatonin by detecting cell viability,apoptosis rate,expressions of apoptosis-related proteins,mitochondrial ROS(mtROS)production,mitochondrial membrane potential(MMP)and adenosine triphosphate(ATP)level.Inhibitors of MAPKs are used to explore which pathway is involved in TEGDMA-induced apoptosis.Finally,the role of the JNK/MAPK pathway is verified using JNK agonists and antagonists.Our results show that melatonin attenuates TEGDMA-induced mDPC6T apoptosis by reducing mtROS production and rescuing MMP and ATP levels.Furthermore,mitochondrial dysfunction and apoptosis are alleviated only by the JNK/MAPK inhibitor SP600125 but not by other MAPK inhibitors.Additionally,melatonin downregulates the expression of phosphorylated JNK and counteractes the activating effects of anisomycin on the JNK/MAPK pathway,mimicking the effects of SP600125.Our findings demonstrate that melatonin protects mDPC6T cells against TEGDMA-induced apoptosis partly through JNK/MAPK and the maintenance of mitochondrial function,offering a novel therapeutic strategy for the prevention of resin monomer-induced dental pulp injury. | Qihao Yu Ruize Hua Bingyang Zhao Dongchao Qiu Chengfei Zhang Shengbin Huang Yihuai Pan | 2024 | Acta Biochimica et Biophysica Sinica2024，56，3： | 0 |
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