BML-111 attenuats acute lung injury induced by intestine ischemia-reperfusion via inhibiting p38 MAPK/NF-κB signaling pathway
10.3969/j.issn.1006-5725.2016.19.008
- VernacularTitle:BML-111通过抑制p38 MAPK／NF-κB通路减轻大鼠肠缺血再灌注早期急性肺损伤
- Author:
Xue HAN
;
Chuwen HU
;
Hui LUO
;
Weifeng YAO
;
Shaoli ZHOU
;
Quehua LUO
;
Mian GE
;
Ning SHEN
- Publication Type:Journal Article
- Keywords:
Acute lung injury;
intestine ischemia reperfusion;
Lipoxin A4 receptor;
BML-111;
Boc-2
- From:
The Journal of Practical Medicine
2016;32(19):3139-3142
- CountryChina
- Language:Chinese
-
Abstract:
Objective This study aims to investigate the effect of Lipoxin A4 receptor on acute lung injury (ALI) induced by intestine ischemia-reperfusion (IIR). Methods Thirty-two 8-week old SD rats were randomly divided into four groups: sham, intestine ischemia-reperfusion (IIR), IIR + BML111 (BML-111), Boc-2 + IIR +BML111 (Boc-2). BML-111 (1 mg/kg) was given intraperitoneally at the onset of reperfusion in the BML-111 and the Boc-2 group. Boc-2 (50 μg/kg) was given intraperitoneally after anesthesia in the Boc-2 group. Rats were subjected to superior mesenteric artery occlusion consisting of 45-min ischemia and 6-h reperfusion, and the sham laparotomy was served as controls. The lung pathology was assayed by the H&E staining. Lung water content was detected using dry/wet ratio. Concentrations of TNF-α, IL-1β, and IL-6 in lung tissue were determined by ELISA. The protein expression of p38 MAPK and NF-κB of lung was assayed by western blot. Results IIR induced serious ALI, with poor lung pathology and increased lung water content, elevation of TNF-α, IL-1β, and IL-6 levels in lung, accompanied with activation of p38 MAPK/NF-κB pathway. However, BML-111 could inhibit the activation of p38 MAPK/NF-κB pathway, leading to the reductions of TNF-α, IL-1β, and IL-6 in lung and attenuation of IIR-induced ALI. Conclusion BML-111 treatment could attenuate inflammation in lung after IIR injury via inactivating the p38 MAPK/NF-κB signaling pathway.
