Dl-3-n-butylphthalide exerts neuroprotective effects by modulating hypoxia-inducible factor 1-alpha ubiquitination to attenuate oxidative stress-induced apoptosis.

Autor:	Li S; Department of Pharmacy, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China., Zhao J; Regenerative Medicine Center, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China., Xi Y; Department of Pharmacy, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China., Ren J; Department of Pharmacy, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China., Zhu Y; Department of Pharmacy, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China., Lu Y; Department of Cardiology, Institute of Cardiovascular Diseases, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China., Dong D; Department of Pharmacy, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China.
Jazyk:	angličtina
Zdroj:	Neural regeneration research [Neural Regen Res] 2023 Nov; Vol. 18 (11), pp. 2424-2428.
DOI:	10.4103/1673-5374.371366
Abstrakt:	Dl-3-n-butylphthalide is used to treat mild and moderate acute ischemic stroke. However, the precise underlying mechanism requires further investigation. In this study, we investigated the molecular mechanism of Dl-3-n-butylphthalide action by various means. We used hydrogen peroxide to induce injury to PC12 cells and RAW264.7 cells to mimic neuronal oxidative stress injury in stroke in vitro and examined the effects of Dl-3-n-butylphthalide. We found that Dl-3-n-butylphthalide pretreatment markedly inhibited the reduction in viability and reactive oxygen species production in PC12 cells caused by hydrogen peroxide and inhibited cell apoptosis. Furthermore, Dl-3-n-butylphthalide pretreatment inhibited the expression of the pro-apoptotic genes Bax and Bnip3. Dl-3-n-butylphthalide also promoted ubiquitination and degradation of hypoxia inducible factor 1α, the key transcription factor that regulates Bax and Bnip3 genes. These findings suggest that Dl-3-n-butylphthalide exhibits a neuroprotective effect on stroke by promoting hypoxia inducible factor-1α ubiquitination and degradation and inhibiting cell apoptosis. Competing Interests: None
Databáze:	MEDLINE
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