Abstract | OBJECTIVE: 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:
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Authors | Chengli Ling, Chang Lei, Manshu Zou, Xiong Cai, Yun Xiang, Yu Xie, Xuran Li, Dan Huang, Yuhong Wang |
Journal | The Journal of international medical research
(J Int Med Res)
Vol. 48
Issue 9
Pg. 300060520945859
(Sep 2020)
ISSN: 1473-2300 [Electronic] England |
PMID | 32993408
(Publication Type: Journal Article)
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Chemical References |
- Neuroprotective Agents
- Apigenin
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Topics |
- Animals
- Apigenin
(pharmacology)
- Apoptosis
- Brain Ischemia
(drug therapy)
- Infarction, Middle Cerebral Artery
(drug therapy)
- Neuroprotective Agents
(pharmacology)
- Oxidative Stress
- Rats
- Reperfusion Injury
(drug therapy)
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