Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

• Main Authors: Yan Zhao, Min Zhang, Ren-Ping Xiong, Xing-Yun Chen, Ping Li, Ya-Lei Ning, Nan Yang, Yan Peng, Yuan-Guo Zhou
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2016-03-01
• Series: Cellular Physiology and Biochemistry
• Subjects: Acute Lung Injury; Somatostatin; Heat Shock Protein 90; Glucocorticoid Receptor
• Online Access: http://www.karger.com/Article/FullText/443079
• ISSN: 1015-8987; 1421-9778

Background/Aims: Although it has been reported that somatostatin (SOM) upregulated the level of 90-kD heat shock protein (Hsp90), which participates in the inflammatory regulation by its client proteins, such as glucocorticoid receptor (GR), it remains unclear if it has a protective role against acute lung injury (ALI). Methods: ALI model was established by the injection of oleic acid (OA) into the tail vein of mice. Lung injury was assessed by histological analysis, lung water content and arterial blood gases. The levels of Hsp90 and GR, the binding capacity and the affinity of GR were examined. Results: It was showed that pretreatment with SOM significantly increased Hsp90 levels and alleviated lung injuries in OA-injected mice. Furthermore, SOM increased the GR expression and improved the affinity of the GR in animals with lung injury. However, little alteration was found in the maximum binding capacity of the GR in mice with or without SOM. Conclusion: The data indicate SOM exerts a protective effect by increasing Hsp90 abundant and further enhancing the affinity of the GR. The beneficial effects of SOM treatment provide a new strategy for modulation of GR efficiency and alleviation of acute lung injury.