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Olaquindox-induced apoptosis is suppressed through p38 MAPK and ROS-mediated JNK pathways in HepG2 cells.
Cell Biol Toxicol. 2013 Aug; 29(4):229-38.CB

Abstract

We investigated mitogen-activated protein kinase (MAPK) pathways as well as reactive oxygen species (ROS) in olaquindox-induced apoptosis. Exposure of HepG2 cells to olaquindox resulted in the phosphorylation of p38 MAPK and c-Jun N-terminal kinases (JNK). To confirm the role of p38 MAPK and JNK, HepG2 cells were pretreated with MAPKs-specific inhibitors prior to olaquindox treatment. Olaquindox-induced apoptosis was significantly potentiated by the JNK inhibitor (SP600125) or the p38 MAPK inhibitor (SB203580). Furthermore, we observed that olaquindox treatment led to ROS generation and that olaquindox-induced apoptosis and ROS generation were both significantly reduced by the antioxidants, superoxide dismutase and catalase. In addition, the levels of phosphorylation of JNK, but not p38 MAPK, were significantly suppressed after pretreatment of the antioxidants, while inhibition of the activations of JNK or p38 MAPK had no effect on ROS generation. This result suggested that ROS may be the upstream mediator for the activation of JNK. Conclusively, our results suggested that apoptosis in response to olaquindox treatment in HepG2 cells might be suppressed through p38 MAPK and ROS-JNK pathways.

Authors+Show Affiliations

Department of Pharmacology and Toxicology, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23812630

Citation

Zhao, Wen-Xia, et al. "Olaquindox-induced Apoptosis Is Suppressed Through P38 MAPK and ROS-mediated JNK Pathways in HepG2 Cells." Cell Biology and Toxicology, vol. 29, no. 4, 2013, pp. 229-38.
Zhao WX, Tang SS, Jin X, et al. Olaquindox-induced apoptosis is suppressed through p38 MAPK and ROS-mediated JNK pathways in HepG2 cells. Cell Biol Toxicol. 2013;29(4):229-38.
Zhao, W. X., Tang, S. S., Jin, X., Zhang, C. M., Zhang, T., Wang, C. C., Sun, Y., & Xiao, X. L. (2013). Olaquindox-induced apoptosis is suppressed through p38 MAPK and ROS-mediated JNK pathways in HepG2 cells. Cell Biology and Toxicology, 29(4), 229-38. https://doi.org/10.1007/s10565-013-9249-y
Zhao WX, et al. Olaquindox-induced Apoptosis Is Suppressed Through P38 MAPK and ROS-mediated JNK Pathways in HepG2 Cells. Cell Biol Toxicol. 2013;29(4):229-38. PubMed PMID: 23812630.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Olaquindox-induced apoptosis is suppressed through p38 MAPK and ROS-mediated JNK pathways in HepG2 cells. AU - Zhao,Wen-Xia, AU - Tang,Shu-Sheng, AU - Jin,Xi, AU - Zhang,Chao-Ming, AU - Zhang,Ting, AU - Wang,Cong-Cong, AU - Sun,Yu, AU - Xiao,Xi-Long, Y1 - 2013/06/30/ PY - 2013/01/22/received PY - 2013/05/31/accepted PY - 2013/7/2/entrez PY - 2013/7/3/pubmed PY - 2014/4/1/medline SP - 229 EP - 38 JF - Cell biology and toxicology JO - Cell Biol Toxicol VL - 29 IS - 4 N2 - We investigated mitogen-activated protein kinase (MAPK) pathways as well as reactive oxygen species (ROS) in olaquindox-induced apoptosis. Exposure of HepG2 cells to olaquindox resulted in the phosphorylation of p38 MAPK and c-Jun N-terminal kinases (JNK). To confirm the role of p38 MAPK and JNK, HepG2 cells were pretreated with MAPKs-specific inhibitors prior to olaquindox treatment. Olaquindox-induced apoptosis was significantly potentiated by the JNK inhibitor (SP600125) or the p38 MAPK inhibitor (SB203580). Furthermore, we observed that olaquindox treatment led to ROS generation and that olaquindox-induced apoptosis and ROS generation were both significantly reduced by the antioxidants, superoxide dismutase and catalase. In addition, the levels of phosphorylation of JNK, but not p38 MAPK, were significantly suppressed after pretreatment of the antioxidants, while inhibition of the activations of JNK or p38 MAPK had no effect on ROS generation. This result suggested that ROS may be the upstream mediator for the activation of JNK. Conclusively, our results suggested that apoptosis in response to olaquindox treatment in HepG2 cells might be suppressed through p38 MAPK and ROS-JNK pathways. SN - 1573-6822 UR - https://www.unboundmedicine.com/medline/citation/23812630/Olaquindox_induced_apoptosis_is_suppressed_through_p38_MAPK_and_ROS_mediated_JNK_pathways_in_HepG2_cells_ L2 - https://doi.org/10.1007/s10565-013-9249-y DB - PRIME DP - Unbound Medicine ER -