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Rosiglitazone inhibits chlorpyrifos-induced apoptosis via modulation of the oxidative stress and inflammatory response in SH-SY5Y cells.
Toxicol Appl Pharmacol. 2014 Jul 15; 278(2):159-71.TA

Abstract

Oxidative stress can lead to expression of inflammatory transcription factors, which are important regulatory elements in the induction of inflammatory responses. One of the transcription factors, nuclear transcription factor kappa-B (NF-κB) plays a significant role in the inflammation regulatory process. Inflammatory cell death has been implicated in neuronal cell death in some neurodegenerative disorders such as Parkinson's disease (PD). In this study, we investigated the molecular mechanisms underlying apoptosis initiated by chlorpyrifos (CPF)-mediated oxidative stress. Based on the cytotoxic mechanism of CPF, we examined the neuroprotective effects of rosiglitazone (RGZ), a peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist, against CPF-induced neuronal cell death. The treatment of SH-SY5Y cells with CPF induced oxidative stress. In addition, CPF activated the p38, JNK and ERK mitogen-activated protein kinases (MAPKs), and induced increases in the inflammatory genes such as COX-2 and TNF-α. CPF also induced nuclear translocation of NF-κB and inhibitors of NF-κB abolished the CPF-induced COX-2 expression. Pretreatment with RGZ significantly reduced ROS generation and enhanced HO-1 expression in CPF-exposed cells. RGZ blocked the activation of both p38 and JNK signaling, while ERK activation was strengthened. RGZ also attenuated CPF-induced cell death through the reduction of NF-κB-mediated proinflammatory factors. Results from this study suggest that RGZ may exert an anti-apoptotic effect against CPF-induced cytotoxicity by attenuation of oxidative stress as well as inhibition of the inflammatory cascade via inactivation of signaling by p38 and JNK, and NF-κB.

Authors+Show Affiliations

Department of Pharmacology, College of Medicine, Hanyang University, Seoul, Republic of Korea; Hanyang Biomedical Research Institute, Seoul, Republic of Korea.Hanyang Biomedical Research Institute, Seoul, Republic of Korea; Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Republic of Korea.Hanyang Biomedical Research Institute, Seoul, Republic of Korea; Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Republic of Korea.Department of Pharmacology, College of Medicine, Hanyang University, Seoul, Republic of Korea; Hanyang Biomedical Research Institute, Seoul, Republic of Korea; Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Republic of Korea. Electronic address: hckoh@hanyang.ac.kr.

Pub Type(s)

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

Language

eng

PubMed ID

24793810

Citation

Lee, Jeong Eun, et al. "Rosiglitazone Inhibits Chlorpyrifos-induced Apoptosis Via Modulation of the Oxidative Stress and Inflammatory Response in SH-SY5Y Cells." Toxicology and Applied Pharmacology, vol. 278, no. 2, 2014, pp. 159-71.
Lee JE, Park JH, Jang SJ, et al. Rosiglitazone inhibits chlorpyrifos-induced apoptosis via modulation of the oxidative stress and inflammatory response in SH-SY5Y cells. Toxicol Appl Pharmacol. 2014;278(2):159-71.
Lee, J. E., Park, J. H., Jang, S. J., & Koh, H. C. (2014). Rosiglitazone inhibits chlorpyrifos-induced apoptosis via modulation of the oxidative stress and inflammatory response in SH-SY5Y cells. Toxicology and Applied Pharmacology, 278(2), 159-71. https://doi.org/10.1016/j.taap.2014.04.021
Lee JE, et al. Rosiglitazone Inhibits Chlorpyrifos-induced Apoptosis Via Modulation of the Oxidative Stress and Inflammatory Response in SH-SY5Y Cells. Toxicol Appl Pharmacol. 2014 Jul 15;278(2):159-71. PubMed PMID: 24793810.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rosiglitazone inhibits chlorpyrifos-induced apoptosis via modulation of the oxidative stress and inflammatory response in SH-SY5Y cells. AU - Lee,Jeong Eun, AU - Park,Jae Hyeon, AU - Jang,Sea Jeong, AU - Koh,Hyun Chul, Y1 - 2014/04/30/ PY - 2013/10/24/received PY - 2014/04/04/revised PY - 2014/04/22/accepted PY - 2014/5/6/entrez PY - 2014/5/6/pubmed PY - 2014/8/6/medline KW - COX-2 KW - Chlorpyrifos KW - NF-κB KW - Reactive oxidative species KW - Rosiglitazone SP - 159 EP - 71 JF - Toxicology and applied pharmacology JO - Toxicol. Appl. Pharmacol. VL - 278 IS - 2 N2 - Oxidative stress can lead to expression of inflammatory transcription factors, which are important regulatory elements in the induction of inflammatory responses. One of the transcription factors, nuclear transcription factor kappa-B (NF-κB) plays a significant role in the inflammation regulatory process. Inflammatory cell death has been implicated in neuronal cell death in some neurodegenerative disorders such as Parkinson's disease (PD). In this study, we investigated the molecular mechanisms underlying apoptosis initiated by chlorpyrifos (CPF)-mediated oxidative stress. Based on the cytotoxic mechanism of CPF, we examined the neuroprotective effects of rosiglitazone (RGZ), a peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist, against CPF-induced neuronal cell death. The treatment of SH-SY5Y cells with CPF induced oxidative stress. In addition, CPF activated the p38, JNK and ERK mitogen-activated protein kinases (MAPKs), and induced increases in the inflammatory genes such as COX-2 and TNF-α. CPF also induced nuclear translocation of NF-κB and inhibitors of NF-κB abolished the CPF-induced COX-2 expression. Pretreatment with RGZ significantly reduced ROS generation and enhanced HO-1 expression in CPF-exposed cells. RGZ blocked the activation of both p38 and JNK signaling, while ERK activation was strengthened. RGZ also attenuated CPF-induced cell death through the reduction of NF-κB-mediated proinflammatory factors. Results from this study suggest that RGZ may exert an anti-apoptotic effect against CPF-induced cytotoxicity by attenuation of oxidative stress as well as inhibition of the inflammatory cascade via inactivation of signaling by p38 and JNK, and NF-κB. SN - 1096-0333 UR - https://www.unboundmedicine.com/medline/citation/24793810/Rosiglitazone_inhibits_chlorpyrifos_induced_apoptosis_via_modulation_of_the_oxidative_stress_and_inflammatory_response_in_SH_SY5Y_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0041-008X(14)00161-6 DB - PRIME DP - Unbound Medicine ER -