Kaempferol Protects Cell Damage in In Vitro Ischemia Reperfusion Model in Rat Neuronal PC12 Cells

• Published in: BioMed research international Vol. 2020; no. 2020; pp. 1 - 10
• Main Authors: Zhou, Ya-ping, Li, Guo-chun
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 2020; Hindawi; John Wiley & Sons, Inc; Hindawi Limited
• Subjects: Acetylation; Animals; Apoptosis; Apoptosis - drug effects; Bioflavonoids; Cell culture; Cell injury; Cell Survival - drug effects; Cell viability; China; Cyclin-dependent kinases; Cytotoxicity; Deoxyribonucleic acid; Deprivation; DNA; Flavones; Flavonoids; Health aspects; Immunoglobulins; Injuries; Ischemia; Kaempferol; Kaempferols - pharmacology; L-Lactate dehydrogenase; Lactate dehydrogenase; Lactic acid; Membranes; Mitochondria; Models, Neurological; Mortality; Nervous system diseases; Neurodegenerative diseases; Neurons; Neurons - metabolism; Neurons - pathology; Oxidative stress; Oxidative Stress - drug effects; PC12 Cells; Penicillin; Pheochromocytoma cells; Proteins; Rats; Reperfusion; Reperfusion Injury - drug therapy; Reperfusion Injury - pathology; Signal Transduction - drug effects; SIRT1 protein; Sirtuin 1 - metabolism; Software; Src Homology 2 Domain-Containing, Transforming Protein 1 - metabolism; Statistical analysis; Stroke; Toxicity; China; United States > US; Switzerland
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2020/2461079

Ischemic cerebral stroke is a severe neurodegenerative disease with high mortality. Ischemia and reperfusion injury plays a fundamental role in ischemic cerebral stroke. To date, the strategy for ischemic cerebral stroke treatment is limited. In the present study, we aimed to investigate the effect of kaempferol (KFL), a natural flavonol, on cell injury induced by oxygen and glucose deprivation (OGD) and reoxygenation (OGD-reoxygenation) in PC12 cells. We found that KFL inhibited OGD-induced decrease of cell viability and the increase of lactate dehydrogenase (LDH) release. OGD-induced activation of mitochondrial dysfunction, mitochondrial apoptotic pathway, and apoptosis was inhibited by KFL. KFL also reduced OGD-induced oxidative stress in PC12 cells. P66shc expression and acetylation were increased by OGD and KFL inhibited these changes. Upregulation of P66shc suppressed KFL-induced decrease of apoptosis, the decrease of LDH release, and the increase of cell viability. Furthermore, KFL inhibited OGD-induced decrease of sirtuin 1 (SIRT1) expression and downregulation of SIRT1 blocked KFL-induced decrease of apoptosis, the decrease of LDH release, and the increase of cell viability. In summary, we identified that KFL exhibited a beneficial effect against OGD-induced cytotoxicity in an ischemia/reperfusion injury cell model. The findings suggest that KFL may be a promising choice for the intervention of ischemic stroke and highlighted the SIRT1/P66shc signaling.