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Cytoprotective effect of chlorogenic acid against hydrogen peroxide-induced oxidative stress in MC3T3-E1 cells through PI3K/Akt-mediated Nrf2/HO-1 signaling pathway.
Oncotarget. 2017 Feb 28; 8(9):14680-14692.O

Abstract

Osteoporosis is a disorder of bone and its development is closely associated with oxidative stress and reactive oxygen species (ROS). Chlorogenic acid (CGA) has potential antioxidant effects and its pharmacological action in osteoblasts is not clearly understood. The present study aimed to clarify the protective effects and mechanisms of CGA on hydrogen peroxide (H2O2)-induced oxidative stress in osteoblast cells. MC3T3-E1 cells were treated with H2O2 to induce oxidative stress model in vitro. Cells were treated with CGA prior to H2O2 exposure, the intracellular ROS production, malondialdehyde content, nitric oxide release and glutathione level were measured. We also investigated the protein levels of heme oxygenase-1 (HO-1), the nuclear translocation of transcription factor NF-erythroid 2-related factor (Nrf2) and the phosphorylation levels of Akt in CGA-treated cells. The results showed that pretreatment of CGA could reverse the inhibition of cell viability and suppress the induced apoptosis and caspase-3 activity. Additionally, it significantly reduced H2O2-induced oxidative damage in a dose-dependent manner. Furthermore, it induced the protein expression of HO-1 together with its upstream mediator Nrf2, and activated the phosphorylation of Akt in MC3T3-E1 cells. LY294002, a PI3K/Akt inhibitor, significantly suppressed the CGA-induced Nrf2 nuclear translocation and HO-1 expression. Reduction of cell death mediated by CGA in presence of H2O2 was significantly inhibited by Zinc protoporphyrin IX (a HO-1 inhibitor) and LY294002. These data demonstrated that CGA protected MC3T3-E1 cells against oxidative damage via PI3K/Akt-mediated activation of Nrf2/HO-1 pathway, which may be an effective drug in treatment of osteoporosis.

Authors+Show Affiliations

College of Veterinary Medicine, China Agricultural University, Beijing 100193, P. R. China.College of Veterinary Medicine, China Agricultural University, Beijing 100193, P. R. China.College of Veterinary Medicine, China Agricultural University, Beijing 100193, P. R. China.College of Veterinary Medicine, China Agricultural University, Beijing 100193, P. R. China.College of Veterinary Medicine, China Agricultural University, Beijing 100193, P. R. China.College of Veterinary Medicine, China Agricultural University, Beijing 100193, P. R. China.College of Veterinary Medicine, China Agricultural University, Beijing 100193, P. R. China.College of Veterinary Medicine, China Agricultural University, Beijing 100193, P. R. China.College of Veterinary Medicine, China Agricultural University, Beijing 100193, P. R. China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28122344

Citation

Han, Dandan, et al. "Cytoprotective Effect of Chlorogenic Acid Against Hydrogen Peroxide-induced Oxidative Stress in MC3T3-E1 Cells Through PI3K/Akt-mediated Nrf2/HO-1 Signaling Pathway." Oncotarget, vol. 8, no. 9, 2017, pp. 14680-14692.
Han D, Chen W, Gu X, et al. Cytoprotective effect of chlorogenic acid against hydrogen peroxide-induced oxidative stress in MC3T3-E1 cells through PI3K/Akt-mediated Nrf2/HO-1 signaling pathway. Oncotarget. 2017;8(9):14680-14692.
Han, D., Chen, W., Gu, X., Shan, R., Zou, J., Liu, G., Shahid, M., Gao, J., & Han, B. (2017). Cytoprotective effect of chlorogenic acid against hydrogen peroxide-induced oxidative stress in MC3T3-E1 cells through PI3K/Akt-mediated Nrf2/HO-1 signaling pathway. Oncotarget, 8(9), 14680-14692. https://doi.org/10.18632/oncotarget.14747
Han D, et al. Cytoprotective Effect of Chlorogenic Acid Against Hydrogen Peroxide-induced Oxidative Stress in MC3T3-E1 Cells Through PI3K/Akt-mediated Nrf2/HO-1 Signaling Pathway. Oncotarget. 2017 Feb 28;8(9):14680-14692. PubMed PMID: 28122344.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cytoprotective effect of chlorogenic acid against hydrogen peroxide-induced oxidative stress in MC3T3-E1 cells through PI3K/Akt-mediated Nrf2/HO-1 signaling pathway. AU - Han,Dandan, AU - Chen,Wei, AU - Gu,Xiaolong, AU - Shan,Ruixue, AU - Zou,Jiaqi, AU - Liu,Gang, AU - Shahid,Muhammad, AU - Gao,Jian, AU - Han,Bo, PY - 2016/11/22/received PY - 2017/01/11/accepted PY - 2017/1/26/pubmed PY - 2017/8/19/medline PY - 2017/1/26/entrez KW - MC3T3-E1 cells KW - Nrf2/HO-1 pathway KW - chlorogenic acid KW - cytoprotection KW - oxidative stress SP - 14680 EP - 14692 JF - Oncotarget JO - Oncotarget VL - 8 IS - 9 N2 - Osteoporosis is a disorder of bone and its development is closely associated with oxidative stress and reactive oxygen species (ROS). Chlorogenic acid (CGA) has potential antioxidant effects and its pharmacological action in osteoblasts is not clearly understood. The present study aimed to clarify the protective effects and mechanisms of CGA on hydrogen peroxide (H2O2)-induced oxidative stress in osteoblast cells. MC3T3-E1 cells were treated with H2O2 to induce oxidative stress model in vitro. Cells were treated with CGA prior to H2O2 exposure, the intracellular ROS production, malondialdehyde content, nitric oxide release and glutathione level were measured. We also investigated the protein levels of heme oxygenase-1 (HO-1), the nuclear translocation of transcription factor NF-erythroid 2-related factor (Nrf2) and the phosphorylation levels of Akt in CGA-treated cells. The results showed that pretreatment of CGA could reverse the inhibition of cell viability and suppress the induced apoptosis and caspase-3 activity. Additionally, it significantly reduced H2O2-induced oxidative damage in a dose-dependent manner. Furthermore, it induced the protein expression of HO-1 together with its upstream mediator Nrf2, and activated the phosphorylation of Akt in MC3T3-E1 cells. LY294002, a PI3K/Akt inhibitor, significantly suppressed the CGA-induced Nrf2 nuclear translocation and HO-1 expression. Reduction of cell death mediated by CGA in presence of H2O2 was significantly inhibited by Zinc protoporphyrin IX (a HO-1 inhibitor) and LY294002. These data demonstrated that CGA protected MC3T3-E1 cells against oxidative damage via PI3K/Akt-mediated activation of Nrf2/HO-1 pathway, which may be an effective drug in treatment of osteoporosis. SN - 1949-2553 UR - https://www.unboundmedicine.com/medline/citation/28122344/Cytoprotective_effect_of_chlorogenic_acid_against_hydrogen_peroxide_induced_oxidative_stress_in_MC3T3_E1_cells_through_PI3K/Akt_mediated_Nrf2/HO_1_signaling_pathway_ L2 - https://www.oncotarget.com/lookup/doi/10.18632/oncotarget.14747 DB - PRIME DP - Unbound Medicine ER -