ArticleBrain sciences2022
Facilitating Mitophagy via Pink1/Parkin2 Signaling Is Essential for the Neuroprotective Effect of β-Caryophyllene against CIR-Induced Neuronal Injury.
Article in Brain sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Terazosin Attenuates Neuronal Pyroptosis by Regulating the Mitochondrial ROS/NLRP3 Inflammasome Axis Through Mitophagy in Cerebral Ischemia-Reperfusion Injury.The Kaohsiung journal of medical sciences · 2026Article
- Astragaloside IV Ameliorates Cerebral Ischemic-Reperfusion Injury via Improving Mitochondrial Function and Inhibiting Neuronal Apoptosis.Current issues in molecular biology · 2025Article
- Investigating the link between microplastic exposure (benzyl butyl phthalate) and neurodegenerative diseases using high-performance computational toxicology.Toxicology research · 2025Article
- Exploring β-caryophyllene: a non-psychotropic cannabinoid's potential in mitigating cognitive impairment induced by sleep deprivation.Archives of pharmacal research · 2025Review
- Role of traditional Chinese medicine monomers in cerebral ischemia/reperfusion injury:a review of the mechanism.Frontiers in pharmacology · 2023Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mitophagy is an important mechanism for maintaining mitochondrial homeostasis through elimination of damaged or dysfunctional mitochondria following cerebral ischemia-reperfusion (CIR) injury. β-Caryophyllene (BCP) is a natural sesquiterpene compound found in the essential oil of plants and has been shown to ameliorate CIR injury. However, whether BCP protects neurons from CIR injury by activating mitophagy is still unclear, and the underlying mechanism remains unknown. In the present study, a mouse neuron HT-22 cell of oxygen-glucose deprivation/reoxygenation (OGD/R) and C57BL/6 male mouse of transient middle artery occlusion followed by 24 h reperfusion (MCAO/R) were established the model of CIR injury. Our results show that BCP remarkably protected against cell death and apoptosis induced by OGD/R, and decreased neurologic injury, infarct volume, and the injury of neurons in CA1 region on MCAO/R mice. In addition, BCP accelerated mitophagy by regulating expression of mitochondrial autophagy marker molecules and the mt-Atp6/Rpl13 ratio (reflecting the relative number of mitochondria), and promoting autophagosome formation compared with OGD/R and MCAO/R groups both in vitro and in vivo. Furthermore, this study revealed that BCP pre-treatment could activate the Pink1/Parkin2 signaling pathway, also with mitophagy activation. To explore the mechanisms, mitochondrial division inhibitor-1 (Mdivi-1) was used to investigate the role of BCP in CIR injury. We found that Mdivi-1 not only decreased BCP-induced facilitation of mitophagy, but also significantly weakened BCP-induced protection against OGD/R and MCAO/R models, which was consistent with levels of Pink1/Parkin2 signaling pathway. Taken together, these results suggest that facilitating mitophagy via Pink1/Parkin2 signaling is essential for the neuroprotective effect of BCP against CIR injury.
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