Luteolin-induced protection of H2O2-induced apoptosis in PC12 cells and the associated pathway
| Autor: | Peng Lin, Wen‑Shi Jiang, Ying‑Jie Zhou, Xing‑Han Tian, Yong‑Shang Yi, Wen‑Jing Cheng |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
chemistry.chemical_classification
Cancer Research Reactive oxygen species Biology medicine.disease medicine.disease_cause Biochemistry Cell biology Superoxide dismutase chemistry.chemical_compound Oncology chemistry Apoptosis Genetics medicine biology.protein Molecular Medicine Molecular Biology Protein kinase B Cell damage Luteolin PI3K/AKT/mTOR pathway Oxidative stress |
| Zdroj: | Molecular Medicine Reports. 12:7699-7704 |
| ISSN: | 1791-3004 1791-2997 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|