Protectin DX increases alveolar fluid clearance in rats with lipopolysaccharide-induced acute lung injury.

Zhuo, Xiao-Jun and Hao, Yu and Cao, Fei and Yan, Song-Fan and Li, Hui and Wang, Qian and Cheng, Bi-Huan and Ying, Bin-Yu and Smith, Fang Gao and Jin, Sheng-Wei (2018) Protectin DX increases alveolar fluid clearance in rats with lipopolysaccharide-induced acute lung injury. Experimental & molecular medicine, 50 (4). p. 49. ISSN 2092-6413. This article is available to all HEFT staff and students via ASK Discovery tool http://tinyurl.com/z795c8c by using their HEFT Athens login IDs

Full text not available from this repository.
Official URL: https://www.nature.com/articles/s12276-018-0075-4

Abstract

Acute respiratory distress syndrome is a life-threatening critical syndrome resulting largely from the accumulation of and the inability to clear pulmonary edema. Protectin DX, an endogenously produced lipid mediator, is believed to exert anti-inflammatory and pro-resolution effects. Protectin DX (5 µg/kg) was injected i.v. 8 h after LPS (14 mg/kg) administration, and alveolar fluid clearance was measured in live rats (n = 8). In primary rat ATII epithelial cells, protectin DX (3.605 × 10 mg/l) was added to the culture medium with LPS for 6 h. Protectin DX improved alveolar fluid clearance (9.65 ± 1.60 vs. 15.85 ± 1.49, p < 0.0001) and decreased pulmonary edema and lung injury in LPS-induced lung injury in rats. Protectin DX markedly regulated alveolar fluid clearance by upregulating sodium channel and Na, K-ATPase protein expression levels in vivo and in vitro. Protectin DX also increased the activity of Na, K-ATPase and upregulated P-Akt via inhibiting Nedd4-2 in vivo. In addition, protectin DX enhanced the subcellular distribution of sodium channels and Na, K-ATPase, which were specifically localized to the apical and basal membranes of primary rat ATII cells. Furthermore, BOC-2, Rp-cAMP, and LY294002 blocked the increased alveolar fluid clearance in response to protectin DX. Protectin DX stimulates alveolar fluid clearance through a mechanism partly dependent on alveolar epithelial sodium channel and Na, K-ATPase activation via the ALX/PI3K/Nedd4-2 signaling pathway.

Item Type: Article
Additional Information: This article is available to all HEFT staff and students via ASK Discovery tool http://tinyurl.com/z795c8c by using their HEFT Athens login IDs
Subjects: WB Practice of medicine
Divisions: Clinical Support > Critical Care
Related URLs:
Depositing User: Mrs Caroline Tranter
Date Deposited: 04 May 2018 13:50
Last Modified: 04 May 2018 13:50
URI: http://www.repository.heartofengland.nhs.uk/id/eprint/1644

Actions (login required)

View Item View Item