Nutritional neuroscience · 2025
The protective role of vitamin B1 in alcohol related headaches induced by disturbance of blood flow and direct cytotoxicity to hippocampal neuron.
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Cao Qinyan, Gao Yang, Li Zhengmao, Xiao Yuyang, Shen Caihong, Xiong Yanfei, Xu Siyuan, Chua Yijin, Li Yanan, Yang Jingpeng, Cao Xiaonian, Meng Lingtong
Аннотация
OBJECTIVES: To evaluate vitamin B1 in alcohol-induced headaches and elucidate its underlying mechanisms and potential preventive applications.
METHODS: In vitro cellular assays assessed the cytotoxicity of alcohol and the protective effects of vitamin B1 on components of the mouse neurovascular units, including endothelial cells, astrocytes, and neurons. Murine models were used to study the effects of alcohol on cerebral blood flow and neurons, as well as the neuroprotective efficacy of vitamin B1. Behavioral tests, immunohistochemistry staining, and two-photon microscope imaging were utilized to quantify physiological and histological changes.
RESULTS: Alcohol demonstrated selective toxicity to hippocampal neurons, distinct from other components of the neurovascular units. It disrupted the dynamics of cerebral blood flow, leading to hypoxic neuronal death. Alcohol's influence on neuron cells contributes to headache pathogenesis. Vitamin B1 significantly attenuated ethanol-mediated cerebral blood flow dysregulation and neuronal damage by reducing reactive oxygen species levels, thereby ameliorating headache-related symptoms.
DISCUSSION: These findings provide new insights into the pathogenesis of alcohol-related headaches and propose vitamin B1 as a viable prophylactic intervention.
METHODS: In vitro cellular assays assessed the cytotoxicity of alcohol and the protective effects of vitamin B1 on components of the mouse neurovascular units, including endothelial cells, astrocytes, and neurons. Murine models were used to study the effects of alcohol on cerebral blood flow and neurons, as well as the neuroprotective efficacy of vitamin B1. Behavioral tests, immunohistochemistry staining, and two-photon microscope imaging were utilized to quantify physiological and histological changes.
RESULTS: Alcohol demonstrated selective toxicity to hippocampal neurons, distinct from other components of the neurovascular units. It disrupted the dynamics of cerebral blood flow, leading to hypoxic neuronal death. Alcohol's influence on neuron cells contributes to headache pathogenesis. Vitamin B1 significantly attenuated ethanol-mediated cerebral blood flow dysregulation and neuronal damage by reducing reactive oxygen species levels, thereby ameliorating headache-related symptoms.
DISCUSSION: These findings provide new insights into the pathogenesis of alcohol-related headaches and propose vitamin B1 as a viable prophylactic intervention.