Clonidine inhibits inflammatory response in lung injury mice through cholinergic anti-inflammatory pathway
10.3969/j.issn.1000-4718.2017.07.021
- VernacularTitle:可乐定通过激活胆碱能抗炎通路抑制肺损伤小鼠炎性反应
- Author:
Yanfeng LIU
;
Zhan LIU
- Keywords:
Clonidine;
Lung injury;
Inflammatory reaction;
Cholinergic anti-inflammatory pathway;
α7 nicotinic acetylcholine receptor;
High-mobility group box protein 1
- From:
Chinese Journal of Pathophysiology
2017;33(7):1283-1287
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To explore the influence of clonidine on inflammatory response in lung injury mice and its possible mechanism.METHODS: Clonidine solution was intravenously injected into the mice with lung injury induced by LPS.The left upper lobe of the lung was collected to detect lung wet/dry weight ratio (W/D) and total lung water content (TLW).The concentrations of IL-6, IL-1β and TNF-α were measured by ELISA.The expression of α7 nicotinic acetylcholine receptor (α7nAChR) and high-mobility group box protein 1 (HMGB1) at mRNA and protein levels was determined by RT-PCR and Western blot.After importing α7nAChR siRNA lentiviral vector or injecting exogenous HMGB1 protein, the inflammatory cytokines were detected.RESULTS: Clonidine attenuated lung injury and inhibited inflammatory reaction.Clonidine promoted the activation of cholinergic anti-inflammatory pathway by promoting α7nAChR expression.Clonidine inhibited HMGB1 expression, which promoted the secretion of IL-6, IL-1β and TNF-α.HMGB1 was negatively regulated by α7nAChR.CONCLUSION: Clonidine functions as an anti-inflammatory reagent to the lung injury mice.The mechanism may be related to activating the cholinergic anti-inflammatory pathway and inhibiting the expression of HMGB1.
