title: IL-5 blocks apoptosis and tau hyperphosphorylation induced by Aβ25-35peptide in PC12 cells.
abstract: The primary features of Alzheimer's disease (AD) are extracellular amyloid plaques consisting mainly of deposits of amyloid β (Aβ) peptides and intracellular neurofibrillary tangles (NFTs). Sets of evidence suggest that interleukin-5 (IL-5) is involved in the pathogenesis of AD. Herein, we investigated the protective role of IL-5 in PC12 cells, to provide new insights into understanding this disease. Western blot was employed to assess the protein levels of Bax and phospho-tau as well as phospho-JAK2; MTT assay was performed to decipher cell viability. Treatment of IL-5 decreased Aβ25-35-induced tau phosphorylation and apoptosis, effects blunted by JAK2 inhibition. IL-5 prevents Aβ25-35-evoked tau protein hyperphosphorylation and apoptosis through JAK2 signaling.
authors.affiliation: Department of Basic Medicine, Luohe Medical College, Luohe, 462002, China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Zhou
authors.affiliation: Department of Basic Medicine, Luohe Medical College, Luohe, 462002, China.
authors.forename: Chaoyan
authors.initials: C
authors.lastname: Li
authors.affiliation: Department of Basic Medicine, Luohe Medical College, Luohe, 462002, China.
authors.forename: Deheng
authors.initials: D
authors.lastname: Li
authors.affiliation: Department of Basic Medicine, Luohe Medical College, Luohe, 462002, China.
authors.forename: Yaping
authors.initials: Y
authors.lastname: Zheng
authors.affiliation: Department of Basic Medicine, Luohe Medical College, Luohe, 462002, China. s17655507933@126.com.
authors.forename: Jin
authors.initials: J
authors.lastname: Wang
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D015848:Interleukin-5 / Q000378:metabolism*; D053666:Interleukin-5 Receptor alpha Subunit / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D053614:Janus Kinase 2 / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000819:agonists / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D016716:PC12 Cells; D010446:Peptide Fragments / Q000378:metabolism*; D010766:Phosphorylation / Q000187:drug effects; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011499:Protein Processing, Post-Translational / Q000187:drug effects; D011759:Pyrrolidines / Q000494:pharmacology; D034622:RNA Interference; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects; D013449:Sulfonamides / Q000494:pharmacology; D016875:tau Proteins / Q000378:metabolism*; D000096926:Benzenesulfonamides
chemical_list: D016229:Amyloid beta-Peptides; D015848:Interleukin-5; D053666:Interleukin-5 Receptor alpha Subunit; D053614:Janus Kinase 2; D009419:Nerve Tissue Proteins; D010446:Peptide Fragments; D047428:Protein Kinase Inhibitors; D011759:Pyrrolidines; D013449:Sulfonamides; D016875:tau Proteins; C489131:Mapt protein, rat; C074636:amyloid beta-protein (25-35); C528327:fedratinib; D000096926:Benzenesulfonamides; C507927:Jak2 protein, rat
keywords: Aβ25–35; IL-5; PC12 cells; Tau