脂氧素A4通过p38 MAPK及Nrf2通路调控气道炎症反应

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Abstract Conclusion: LXA4 may attenuate Objective: To investigate the effect and mechanism of Lipoxin A4 (LXA4) on inflammatory response induced by lipopolysaccharide (LPS) in BEAS-2B cells. Methods: Cultured BEAS-2B cells in logarithmic growth phase were divided into 3 groups: control group (group A, non-treatment), LPS group (group B, incubated with 100 ng/mL LPS for 24 h), LPS+LXA4 treatment group (group C, pretreated with 100 nmol/L LXA4 for 30 min and incubated with 100 ng/mL LPS for 24 h). The mRNA levels of IL-6, IL-1β, heme oxygenase (HO-1) and NAD (P) H: quinone oxidoreductase (NQO-1) were detected by qPCR. The expression of reactive oxygen species (ROS) was detected by flow cytometric analysis. Glutathione (GSH) was measured by a GSH assay kit. Moreover, we investigated the effects of LXA4 on LPS-induced phosphorylation of p38 mitogen-activated protein kinases (MAPK) as well as nuclear translocation and phosphorylation of Nrf2. Results: Compared with group A, the mRNA expressions of IL-6, IL-1β and the level of ROS in group B were significantly increased (P<0.05), while the mRNA level of HO-1 in cells was significantly decreased (P<0.01). Nuclear translocation and phosphorylation of Nrf2 were reduced (P<0.05) and phosphorylation of p38 MAPK was significantly increased (P<0.01) after LPS stimulation. In contrast, in LXA4 treatment group, the above changes were reversed (P<0.05); besides, GSH activity and the mRNA level of NQO-1 were elevated (P<0.05). Conclusion: LXA4 may attenuate Objective: To investigate the effect and mechanism of Lipoxin A4 (LXA4) on inflammatory response induced by lipopolysaccharide (LPS) in BEAS-2B cells. Methods: Cultured BEAS-2B cells in logarithmic growth phase were divided into 3 groups: control group (group A, non-treatment), LPS group (group B, incubated with 100 ng/mL LPS for 24 h), LPS+LXA4 treatment group

Received: 12 March 2018

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	ZHUO Leying
	WU Zhenjie
	YU Xiang
	ZHOU Meixi
	LI Chengye
	OUYANG Jinsheng
	LIN Qibin
	CAI Chang.

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https://xb.wmu.edu.cn/EN/ OR https://xb.wmu.edu.cn/EN/Y2018/V48/I6/418

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