Abstract

Reducing inflammation can effectively relieve acute lung injury (ALI). Objective. To test whether keratinocyte growth factor-2 (KGF-2) can reduce oleic acid-induced inflammation in ALI of rats and explore its possible mechanism. Methods. 45 Sprague-Dawley rats were randomly divided into control group, ALI group, and ALI + KGF-2 group. The animal model of acute lung injury was established by injecting 0.1 mL/kg oleic acid into the tail vein of rats. Rats in the control group were injected with equal volume of normal saline (NS). Each group needs pretreatment 72 hours before the preparation of the acute lung injury model. The control group and ALI group were instilled with 5 ml/kg NS through the airway, and the same amount of KGF-2 was instilled in the ALI + KGF-2 group. It takes 8 hours to successfully prepare the ALI model. Observe the pathological changes of lung tissue through light microscopy, ultrastructural changes through electron microscopy, and the lung wettability/dry weight (w/d) ratio and lung permeability index (LPI). By detecting changes in inflammatory factors in lung tissue and changes in the number of BALF cells, the changes in inflammation in each group were observed. The expressions of Wnt5a, β-catenin, and APC in lung tissue were detected by immunohistochemistry and Western blot. The changes of key proteins in Wnt/β-catenin signaling pathway in the lung tissue of each group were observed. Result. Compared with the ALI group, after KGF-2 pretreatment, the degree of lung injury was reduced, the expression of inflammatory factors was reduced, and the number of red blood cells and white blood cells in BALF was reduced. It can also be observed that the expression of Wnt5a, β-catenin, and APC, a key protein in the Wnt/β-catenin signaling pathway, is reduced. The analysis showed that the number of inflammatory factors, red blood cells, and white blood cells in BALF was positively correlated with the expression of Wnt5a, β-catenin, and APC. Conclusion. KGF-2 may reduce the inflammatory response in ALI induced by oleic acid by regulating key proteins in the Wnt/β-catenin signaling pathway.

Highlights

  • Shao Tenghao,1 Chen Ning,1 Wang Shenghai,1 Sun Qinlong,1 Wu Jiaqian,1 Wang Kuo,1 Yu Zhanbiao,1 and Ma Xigang 2

  • It can be observed that the expression of Wnt5a, β-catenin, and APC, a key protein in the Wnt/β-catenin signaling pathway, is reduced. e analysis showed that the number of inflammatory factors, red blood cells, and white blood cells in bronchoalveolar lavage fluid (BALF) was positively correlated with the expression of Wnt5a, β-catenin, and APC

  • Forty-five SD rats were randomly divided into three groups: control group, acute lung injury (ALI) group, and ALI + keratinocyte growth factor-2 (KGF-2) group. e preparation of the rat ALI model was completed by injecting 0.1 mL/kg oleic acid (Sigma, USA) into the tail vein of the rat. e control group was injected with 0.1 mL/kg saline (NS) in the tail vein as a control. ree groups were instilled by tracheal infusion 72 h before the tail vein injection. e ALI + KGF-2 group was infused with 5 mg/kg of KGF-2, and the control group and ALI group were infused with 5 mg/kg of normal saline (NS)

Read more

Summary

Introduction

By detecting changes in inflammatory factors in lung tissue and changes in the number of BALF cells, the changes in inflammation in each group were observed. E changes of key proteins in Wnt/β-catenin signaling pathway in the lung tissue of each group were observed. Compared with the ALI group, after KGF-2 pretreatment, the degree of lung injury was reduced, the expression of inflammatory factors was reduced, and the number of red blood cells and white blood cells in BALF was reduced. KGF-2 may reduce the inflammatory response in ALI induced by oleic acid by regulating key proteins in the Wnt/β-catenin signaling pathway. E third step is to detect whether KGF-2 has a regulatory effect on key proteins in the Wnt/β-catenin signaling pathway. The mechanism of action of KGF-2 on ALI is explored

Methods
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.