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Ursolic acid ameliorates traumatic brain injury in mice by regulating microRNA-141-mediated PDCD4/PI3K/AKT signaling pathway

神经保护 神经炎症 下调和上调 氧化应激 创伤性脑损伤 蛋白激酶B 莫里斯水上航行任务 PI3K/AKT/mTOR通路 炎症 细胞凋亡 熊果酸 药理学 医学 神经科学 生物 免疫学 内科学 生物化学 海马体 精神科 基因 植物
作者
Hongyun Zhang,Zhenyi Xing,Jie Zheng,Jiandang Shi,Can Cui
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:120: 110258-110258 被引量:7
标识
DOI:10.1016/j.intimp.2023.110258
摘要

Neuronal apoptosis and inflammation are the key pathogenic features of secondary brain injury, which results in the neurological impairment that traumatic brain injury (TBI) patients experience. Ursolic Acid (UA) has been shown to have neuroprotective properties against brain damage, however, detailed mechanisms have not been fully disclosed. Research on brain-related microRNAs (miRNAs) has opened up new possibilities for the neuroprotective treatment of UA by manipulating miRNAs. The present study was designed to investigate the impact of UA on neuronal apoptosis and the inflammatory response in TBI mice. The mice's neurologic condition was assessed using the modified neurological severity score (mNSS) and the learning and memory abilities were assessed using the Morris water maze (MWM). Cell apoptosis, oxidative stress, and inflammation were utilized to examine the impact of UA on neuronal pathological damage. miR-141-3p was selected to evaluate whether UA influences miRNAs in a way that has neuroprotective benefits. The results showed that UA markedly decreased brain edema and neuronal mortality through oxidative stress and neuroinflammation in TBI mice. Using data from the GEO database, we found that miR-141-3p was considerably downregulated in TBI mice and that this downregulation was reversed by UA treatment. Further studies have shown that UA regulates miR-141-3p expression to exhibit its neuroprotective effect in mouse models and cell injury models. Then, miR-141-3p was discovered to directly target PDCD4 in TBI mice and neurons, a well-known PI3K/AKT pathway regulator in the neurons. Most importantly, the upregulation of phosphorylated (p)-AKT and p-PI3K provided the most compelling evidence that UA reactivated the PI3K/AKT pathway in the TBI mouse model, which was through regulating miR-141-3p. Our findings support the notion that UA can improve TBI by modulating miR-141 mediated PDCD4/PI3K/AKT signaling pathway.
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