Crocetin protects mouse brain from apoptosis in traumatic brain injury model through activation of autophagy

被引：0

作者：

Chen, Shan ^{[1
]}

Luo, Xinghong ^{[1
]}

Yang, Liu ^{[1
]}

Luo, Liang ^{[1
]}

Hu, Zhen ^{[1
]}

Wang, Jianglan ^{[1
]}

机构：

[1] Wuhan Caidian Dist Peoples Hosp, Dept Lab, 111 Success Ave, Wuhan, Hubei, Peoples R China

来源：

BRAIN INJURY | 2024年 / 38卷 / 07期

关键词：

Traumatic brain injury; crocetin; autophagy; apoptosis; neuroinflammation; INDUCED INFLAMMATION; CELL-DEATH; PATHWAY; MICE; PATHOPHYSIOLOGY; NEUROPROTECTION; ENHANCEMENT; CONTRIBUTES; ACID; RATS;

D O I：

10.1080/02699052.2024.2324022

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

BackgroundAutophagy is recognized as a promising therapeutic target for traumatic brain injury (TBI). Crocetin is an aglycone of crocin naturally occurring in saffron and has been found to alleviate brain injury diseases. However, whether crocetin affects autophagy after TBI remains unknown. Therefore, we explore crocetin roles in autophagy after TBI.MethodsWe used a weight-dropped model to induce TBI in C57BL/6J mice. Neurological severity scoring (NSS) and grip tests were used to evaluate the neurological level of injury. Brain edema, neuronal apoptosis, neuroinflammation and autophagy were detected by measurements of brain water content, TUNEL staining, ELISA kits and western blotting.ResultsCrocetin ameliorated neurological dysfunctions and brain edema after TBI. Crocetin reduced neuronal apoptosis and neuroinflammation and enhanced autophagy after TBI.ConclusionCrocetin alleviates TBI by inhibiting neuronal apoptosis and neuroinflammation and activating autophagy.

引用

页码：524 / 530

页数：7

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