title: Gossypium herbaceam L. extracts ameliorate disequilibrium of IL-1RA/IL-1β ratio to attenuate inflammatory process induced by amyloid β in rats.
abstract: A chronic inflammatory response possibly mediated by Amyloid β (Aβ) is believed to be a major factor in the pathology of Alzheimer's disease (AD). Studies suggest that the mediators of the inflammatory response, which might contribute to brain damage, involve cytokines, such as IL-1β. IL-1β could play an important part in the development of pathologic conditions. There is also an endogenous interleukin-1 receptor antagonist (IL-1RA) in IL-1 family, which could prevent the actions of IL-1β by competing for receptor binding without inducing any signal transduction. Therefore, the balance of IL-1β vs IL-1RA is a critical parameter in determining not only whether excessive host inflammation will occur, but also the degree of subsequent host cell damage and associated toxicity. In our previous study, it has been determined that the anti-inflammatory action of Gossypium herbaceam L. extracts (GHE) was involved in its neuroprotection. However, the effects of GHE on IL-1β and IL-1RA have not been clearly defined in the experimental rat model of AD induced by Aβ. Therefore, the current study is performed to evaluate whether GHE could affect the disequilibrium of IL-1RA/IL-1β ratio in the hippocampus of rats after Aβ treatment. Subsequently, we further identify that GHE could efficaciously promote Akt and GSK3β phosphorylation, and thereby contribute to IL-1β release decrease as well as a concurrent increase in the level of IL-1RA through NF-κB and MAPK pathways. As a consequence, GHE is potentially beneficial to maintain the endogenous IL-1RA/ IL-1β balance in the hippocampus of rats and it might be a potential agent to ameliorate inflammatory process in AD.
authors.affiliation: School of Basic Medicine, Peking Union Medical College & Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing 100005, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Ji
authors.forename: Cai
authors.initials: C
authors.lastname: Song
authors.forename: Haji Akber
authors.initials: HA
authors.lastname: Aisa
authors.forename: Nan
authors.initials: N
authors.lastname: Yang
authors.forename: Yan-Yong
authors.initials: YY
authors.lastname: Liu
authors.forename: Qing
authors.initials: Q
authors.lastname: Li
authors.forename: Hai-Bo
authors.initials: HB
authors.lastname: Zhu
authors.forename: Ping-Ping
authors.initials: PP
authors.lastname: Zuo
mesh_terms: D000544:Alzheimer Disease / Q000276:immunology / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D015153:Blotting, Western; D024202:Electrophoretic Mobility Shift Assay; D004797:Enzyme-Linked Immunosorbent Assay; D003368:Gossypium; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D053590:Interleukin 1 Receptor Antagonist Protein / Q000276:immunology / Q000378:metabolism; D053583:Interleukin-1beta / Q000276:immunology / Q000378:metabolism; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010936:Plant Extracts / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects* / Q000276:immunology
chemical_list: D016229:Amyloid beta-Peptides; D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta; D018696:Neuroprotective Agents; D010936:Plant Extracts