Protective effect of Cordyceps sinensis extract on lipopolysaccharide-induced acute lung injury in mice.

Shuiqiao Fu,Wenqiao Yu,Jun Hu,Weina Lu

doi:10.1042/bsr20190789

Abstract

Background: To study the protective effect of Cordyceps sinensis extract (Dong Chong Xia Cao in Chinese [DCXC]) on experimental acute lung injury (ALI) mice.Methods and results: ALI model was induced by intratracheal-instilled lipopolysaccharide (LPS, 2.4 mg/kg) in BALB/c male mice. The mice were administrated DCXC (ig, 10, 30, 60 mg/kg) in 4 and 8 h after receiving LPS. Histopathological section, wet/dry lung weight ratio and myeloperoxidase activity were detected. Bronchoalveolar lavage fluid (BALF) was collected for cell count, the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and nitric oxide (NO) in BALF was detected by ELISA, the protein and mRNA expression of nuclear factor-κB p65 (NF-κB p65), inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung tissue was detected by Western blot and RT-PCR. The result showed that DCXC could reduce the degree of histopathological injury, wet/dry weight ratio (W/D ratio) and myeloperoxidase activity (P<0.05) with a dose-dependent manner. The increased number of total cells, neutrophils and macrophages in BALF were significantly inhibited by DCXC treatment (P<0.05). The increased levels of TNF-α, IL-1β, IL-6 and NO in BALF after LPS administration was significantly reduced by DCXC (P<0.05). In addition, the increased protein and mRNA levels of iNOS, COX-2 and NF-κB p65 DNA binding ability in LPS group were dose-dependently reduced by DCXC treatment (P<0.05).Conclusion: DCXC could play an anti-inflammatory and antioxidant effect on LPS-induced ALI through inhibiting NF-κB p65 phosphorylation, and the expression of COX-2 and iNOS in lung. The result showed that DCXC has a potential protective effect on the ALI.

Highlights

Acute lung injury (ALI) and its severest stage acute respiratory distress syndrome (ARDS) will lead to a multiple organ dysfunction syndromes (MODS) in lung tissue [1]
The specific manifestations of acute lung injury (ALI) are the increase of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β), as well as the release of other mediators caused by cascade amplification, resulting in increased pulmonary capillary permeability, interstitial edema, neutrophil exudation and a series of inflammation [5,6]
Previous studies have shown that the pathological changes of lung tissue can reflect the ALI induced by LPS [22]

Summary

Introduction

Acute lung injury (ALI) and its severest stage acute respiratory distress syndrome (ARDS) will lead to a multiple organ dysfunction syndromes (MODS) in lung tissue [1]. ALI is a common acute and critical disease in clinic It has a complicated pathogenesis, the pathological characterizations of ALI are pulmonary edema and atelectasis, which will lead to an inflammation and increased permeability of lung tissue, and this increased permeability will lead to a gas exchange dysfunction [3,4]. The result showed that DCXC could reduce the degree of histopathological injury, wet/dry weight ratio (W/D ratio) and myeloperoxidase activity (P

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