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Inhibition of MAPKs Signaling Pathways Prevents Acrolein-Induced Neurotoxicity in HT22 Mouse Hippocampal Cells.
Biol Pharm Bull. 2019 Apr 01; 42(4):617-622.BP

Abstract

Activation of mitogen-activated protein kinases (MAPKs) in neurons may underlie the pathogenesis of Alzheimer's disease (AD). Acrolein, a ubiquitous pollutant, has been reported to implicate in the etiology of AD. Our previous data showed that acrolein changed the levels of key AD-associated proteins, including advanced glycation end products (RAGE), A-disintegrin and metalloprotease (ADAM-10), and beta-site amyloid-beta peptide cleaving enzyme 1 (BACE-1). In this study, we investigated whether acrolein-induced alterations of AD-associated proteins are relevant to MAPKs activation, and strategies to inhibit MAPKs activation yield benefits to acrolein-induced neurotoxicity in HT22 mouse hippocampal cells. We found that acrolein activated MAPKs signaling pathways to mediate cells apoptosis, and then altered the levels of AD-associated proteins ADAM-10, BACE-1 and RAGE. Inhibitors of MAPKs signaling pathways attenuated the cells death and restored the proteins levels of ADAM-10, BACE-1 and RAGE in varying degrees induced by acrolein. Taken together, activated MAPKs signaling pathways should be underlying the pathology of acrolein-induced neuronal disorders. Inhibitors of MAPKs pathways might be promising agents for acrolein-related diseases, such as AD.

Authors+Show Affiliations

Department of Traditional Chinese Medicine, the First Affiliated Hospital, Sun Yat-sen University.Department of Traditional Chinese Medicine, the First Affiliated Hospital, Sun Yat-sen University.Department of Traditional Chinese Medicine, the First Affiliated Hospital, Sun Yat-sen University.Department of Traditional Chinese Medicine, the Eastern Hospital of the First Affiliated Hospital, Sun Yat-sen University.Department of Traditional Chinese Medicine, the First Affiliated Hospital, Sun Yat-sen University.Department of Traditional Chinese Medicine, the First Affiliated Hospital, Sun Yat-sen University.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30700647

Citation

Liu, MengTing, et al. "Inhibition of MAPKs Signaling Pathways Prevents Acrolein-Induced Neurotoxicity in HT22 Mouse Hippocampal Cells." Biological & Pharmaceutical Bulletin, vol. 42, no. 4, 2019, pp. 617-622.
Liu M, Huang Y, Qin J, et al. Inhibition of MAPKs Signaling Pathways Prevents Acrolein-Induced Neurotoxicity in HT22 Mouse Hippocampal Cells. Biol Pharm Bull. 2019;42(4):617-622.
Liu, M., Huang, Y., Qin, J., Wang, Y., Ke, B., & Yang, Y. (2019). Inhibition of MAPKs Signaling Pathways Prevents Acrolein-Induced Neurotoxicity in HT22 Mouse Hippocampal Cells. Biological & Pharmaceutical Bulletin, 42(4), 617-622. https://doi.org/10.1248/bpb.b18-00715
Liu M, et al. Inhibition of MAPKs Signaling Pathways Prevents Acrolein-Induced Neurotoxicity in HT22 Mouse Hippocampal Cells. Biol Pharm Bull. 2019 Apr 1;42(4):617-622. PubMed PMID: 30700647.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of MAPKs Signaling Pathways Prevents Acrolein-Induced Neurotoxicity in HT22 Mouse Hippocampal Cells. AU - Liu,MengTing, AU - Huang,YingJuan, AU - Qin,Jian, AU - Wang,YuanYuan, AU - Ke,Bin, AU - Yang,YuBin, Y1 - 2019/01/29/ PY - 2019/2/1/pubmed PY - 2019/7/17/medline PY - 2019/2/1/entrez KW - Alzheimer’s disease KW - acrolein KW - inhibitor KW - mitogen-activated protein kinase SP - 617 EP - 622 JF - Biological & pharmaceutical bulletin JO - Biol Pharm Bull VL - 42 IS - 4 N2 - Activation of mitogen-activated protein kinases (MAPKs) in neurons may underlie the pathogenesis of Alzheimer's disease (AD). Acrolein, a ubiquitous pollutant, has been reported to implicate in the etiology of AD. Our previous data showed that acrolein changed the levels of key AD-associated proteins, including advanced glycation end products (RAGE), A-disintegrin and metalloprotease (ADAM-10), and beta-site amyloid-beta peptide cleaving enzyme 1 (BACE-1). In this study, we investigated whether acrolein-induced alterations of AD-associated proteins are relevant to MAPKs activation, and strategies to inhibit MAPKs activation yield benefits to acrolein-induced neurotoxicity in HT22 mouse hippocampal cells. We found that acrolein activated MAPKs signaling pathways to mediate cells apoptosis, and then altered the levels of AD-associated proteins ADAM-10, BACE-1 and RAGE. Inhibitors of MAPKs signaling pathways attenuated the cells death and restored the proteins levels of ADAM-10, BACE-1 and RAGE in varying degrees induced by acrolein. Taken together, activated MAPKs signaling pathways should be underlying the pathology of acrolein-induced neuronal disorders. Inhibitors of MAPKs pathways might be promising agents for acrolein-related diseases, such as AD. SN - 1347-5215 UR - https://www.unboundmedicine.com/medline/citation/30700647/Inhibition_of_MAPKs_Signaling_Pathways_Prevents_Acrolein_Induced_Neurotoxicity_in_HT22_Mouse_Hippocampal_Cells_ L2 - https://dx.doi.org/10.1248/bpb.b18-00715 DB - PRIME DP - Unbound Medicine ER -