title: Luteolin-induced protection of H₂O₂-induced apoptosis in PC12 cells and the associated pathway.
abstract: Increasing evidence has indicated that the generation of reactive oxygen species (ROS) contributes to H2O2‑induced nerve injury. This may result in oxidative stress that leads to cell damage or death. Dietary or pharmaceutical augmentation of the endogenous antioxidant defense capacity is a potential means by which to prevent ROS‑induced damage. The aim of the current study was to investigate the effect of luteolin on H2O2‑induced cell apoptosis in cultured rat pheochromocytoma cells (PC12 cells) and to investigate the role of the phosphatidylinositol‑3‑kinase (PI3K)/protein kinase B (Akt) pathway on H2O2‑induced apoptosis. The results demonstrated that luteolin was able to inhibit the reduction in cell viability induced by H2O2. In addition, luteolin reduced ROS generation and lactate dehydrogenase release in H2O2‑treated PC12 cells. The levels of superoxide dismutase and glutathione peroxidase activity were increased following treatment with luteolin, however malondialdehyde levels were observed to be reduced. Additionally, luteolin increased the Bcl‑2/Bax ratio and enhanced Akt phosphorylation. However, these alterations were attenuated by pretreatment with an inhibitor of the PI3K/Akt pathway. In conclusion, luteolin inhibited H2O2‑induced apoptosis via reducing ROS levels and activating the PI3K/Akt pathway.
authors.affiliation: Department of Intensive Care Unit, Yuhuangding Hospital Affiliated to Qingdao University, Yantai, Shandong 264000, P.R. China.
authors.forename: Peng
authors.initials: P
authors.lastname: Lin
authors.affiliation: Department of Intensive Care Unit, Yuhuangding Hospital Affiliated to Qingdao University, Yantai, Shandong 264000, P.R. China.
authors.forename: Xing-Han
authors.initials: XH
authors.lastname: Tian
authors.affiliation: Department of Neurology, Seaport Hospital Shandong, Yantai, Shandong 264000, P.R. China.
authors.forename: Yong-Shang
authors.initials: YS
authors.lastname: Yi
authors.affiliation: Department of Intensive Care Unit, People's Hospital of Yangshuo County, Yangshuo, Guangxi 541900, P.R. China.
authors.forename: Wen-Shi
authors.initials: WS
authors.lastname: Jiang
authors.affiliation: Department of Neurology, Seaport Hospital Shandong, Yantai, Shandong 264000, P.R. China.
authors.forename: Ying-Jie
authors.initials: YJ
authors.lastname: Zhou
authors.affiliation: Department of Neurology, No. 1 People's Hospital of Jining, Jining, Shandong 272000, P.R. China.
authors.forename: Wen-Jing
authors.initials: WJ
authors.lastname: Cheng
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D006861:Hydrogen Peroxide / Q000378:metabolism*; D047311:Luteolin / Q000494:pharmacology*; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D016716:PC12 Cells; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000975:Antioxidants; D018696:Neuroprotective Agents; D006861:Hydrogen Peroxide; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D047311:Luteolin