Neuroprotective effect of apigenin against cerebral ischemia/reperfusion injury. Issue 9 (September 2020)

• Record Type: Journal Article
• Authors: Ling, Chengli; Lei, Chang; Zou, Manshu; Cai, Xiong; Xiang, Yun; Xie, Yu; Li, Xuran; Huang, Dan; Wang, Yuhong
• Is Part Of: Journal of international medical research. Volume 48:Issue 9(2020)
• Publication Date: 2020-09
• Subjects: Cerebral ischemia/reperfusion -- neuropharmacology -- apigenin -- flavonoids -- PC12 cell model -- oxidative stress -- mitochondria -- middle cerebral artery occlusion rat model; Medicine -- Periodicals; Pharmacology -- Periodicals; 610.5
• DOI: 10.1177/0300060520945859
• Languages: English
• ISSNs: 0300-0605

Abstract

Objective: The therapeutic efficacy of apigenin in PC12 cells and rats remains uncertain. The aim of this study was to investigate the neuroprotective effects of apigenin against cerebral ischemia/reperfusion injury, both in vitro and in vivo . Methods: We first treated PC12 cells with cobalt chloride (CoCl2 ) to create a model of oxidative stress injury. Cell viability was then determined using a multifunctional microplate reader. In addition, reactive oxygen species (ROS) levels, apoptosis, and mitochondrial membrane potentials (MMPs) were examined using high-content cytometer analysis. The efficacy of apigenin treatment was also analyzed in a rat middle cerebral artery occlusion (MCAO) model using TTC staining and neurological deficit scores. Results: The half-inhibitory concentration of CoCl2 was 1.2 mM. Pretreatment with 10 µg ⋅ mL −1 apigenin significantly enhanced cell viability, reduced ROS levels, alleviated apoptosis, and improved MMP in PC12 cells with CoCl2 -induced injury in vitro . In addition, apigenin treatment in vivo significantly improved neurological deficit scores and reduced infarct areas in MCAO rats. These results suggest that the neuroprotective mechanisms of apigenin may be related to mitochondrial activation. Conclusions: Apigenin had excellent neuroprotective effects for the treatment of cerebral ischemia/reperfusion injury in vitro and in vivo.