Effect of Toll-like receptor nano-inhibitor P12 on pulmonary inflammation in acute lung injury mice
10.3969/j.issn.1674-8115.2018.08.006
- Author:
Wei GAO
1
Author Information
1. Department of Pulmonary and Critical Care Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine
- Publication Type:Journal Article
- Keywords:
Acute lung injury (ALI);
Multi-target anti-inflammatory activity;
Nano-inhibitor;
Nanoparticle;
Toll-like receptor (TLR)
- From:
Journal of Shanghai Jiaotong University(Medical Science)
2018;38(8):888-893
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect of the Toll-like receptor (TLR) nano-inhibitor P12 on THP-1 derived macrophages and acute lung injury (ALI) mouse model induced by lipopolysaccharides (LPS). Methods: In in vitro experiments, THP-1 cells were differentiated into macrophage-like cells and then treated with LPS in the absence and presence of P12. After 24 h incubation, medium was collected to quantify the secretion of pro-inflammatory cytokines using enzyme-linked immunosorbent assay (ELISA). Six- to eight-week-old C57BL/6 mice were randomly divided into three groups, i.e. PBS control, LPS challenge and P12 pretreatment plus LPS. The bronchial alveolar lavage fluid (BALF) and lung tissue of each mouse were collected, and the acute inflammatory response within lung was evaluated by total cell counts, differential cell counts and ELISA. Pathological injury scores in ALI mice were assessed with hematoxylin and eosin (H-E) staining of lung tissue sections under microscope. Results: In THP-1 derived macrophages, P12 significantly inhibited LPS-induced inflammatory cytokine production. In the LPS-induced ALI mouse model, P12 significantly attenuated the acute inflammatory response and alveolar damage in lung, including reducing the number of total cells and neutrophils in BALF, decreasing the expression of chemokine production (KC and CCL-2), and lowering lung injury scores. Conclusion: P12 exhibits potent anti-inflammatory activity in THP-1 derived macrophages and in the LPS-induced ALI mouse model, providing new concepts for the early treatment of ALI.
