首页|Melatonin alleviates valproic acid-induced neural tube defects by modulating Src/PI3K/ERK signaling and oxidative stress

Melatonin alleviates valproic acid-induced neural tube defects by modulating Src/PI3K/ERK signaling and oxidative stress

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Neural tube defects(NTDs)represent a developmental disorder of the nervous system that can lead to significant disability in children and impose substantial social burdens.Valproic acid(VPA),a widely prescribed first-line antiepileptic drug for epilepsy and various neurological conditions,has been associated with a 4-fold increase in the risk of NTDs when used during pregnancy.Consequently,urgent efforts are required to identify innovative pre-vention and treatment approaches for VPA-induced NTDs.Studies have demonstrated that the disruption in the delicate balance between cell proliferation and apoptosis is a crucial factor contributing to NTDs induced by VPA.Encouragingly,our current data reveal that melatonin(MT)significantly inhibits apoptosis while promoting the restoration of neuroepithelial cell proliferation impaired by VPA.Moreover,further investigations demonstrate that MT substantially reduces the incidence of neural tube malformations resulted from VPA exposure,primarily by suppressing apoptosis through the modulation of intracellular reactive oxygen species levels.In addition,the Src/PI3K/ERK signaling pathway appears to play a pivotal role in VPA-induced NTDs,with significant inhibition ob-served in the affected samples.Notably,MT treatment successfully reinstates Src/PI3K/ERK signaling,thereby offering a potential underlying mechanism for the protective effects of MT against VPA-induced NTDs.In summary,our current study substantiates the considerable protective potential of MT in mitigating VPA-triggered NTDs,thereby offering valuable strategies for the clinical management of VPA-related birth defects.

melatoninvalproic acidneural tube defectsreactive oxygen species

Yuxiang Liang、Ying Wang、Xiao Zhang、Shanshan Jin、Yuqian Guo、Zhaowei Yu、Xinrui Xu、Qizhi Shuai、Zihan Feng、Binghong Chen、Ting Liang、Ruifang Ao、Jianting Li、Juan Zhang、Rui Cao、Hong Zhao、Zhaoyang Chen、Zhizhen Liu、Jun Xie

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Department of Biochemistry and Molecular Biology,Shanxi Key Laboratory of Birth Defect and Cell Regeneration,MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention,Shanxi Medical University,Taiyuan 030001,China

Experimental Animal Center of Shanxi Medical University,Shanxi Key Laboratory of Human Disease and Animal Models,Taiyuan 030001,China

School of Pharmacy,Shanxi Medical University,Taiyuan 030001,China

国家重点研发计划山西省自然科学基金山西省自然科学基金山西省自然科学基金Science and Technology Innovation Plan of Colleges and Universities of Education Department of Shanxi ProvinceOpen Fund from Key Laboratory of Cellular Physiology(Shanxi Medical University)教育部项目Central Guidance on Local Science and Technology Development Fund for Shanxi ProvinceFund for Shanxi Key Subjects Construction(FSKSC)国家自然科学基金

2021YFC23016032021030212404120210302123347202103021246162020L0182CELLPHYSIOL/SXMU-2021-CPOF202108YDZJSX2021B00882203221

2024

10.3724/abbs.2023234

生物化学与生物物理学报(英文版)
中国科学院上海生物化学研究所

生物化学与生物物理学报(英文版)

CSTPCD
影响因子：0.772
ISSN：1672-9145
年,卷(期)：2024.56(1)
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