Chun-ling Chen1, Tao-ping Li, Li-hua Zhu. 1. Department of Respiratory Diseases, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. ccl1202@163.com
Abstract
OBJECTIVE: To investigate the relationship between aquaporin 4 (AQP4) in alveolar type II (AT-II) cells and MAPK signaling pathway in rats with early-stage oleic acid-induced acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). METHODS: Three groups of rats, namely the normal control, ALI and U0126 treatment group were used in this study. After oleic acid-induced ALI in the latter two groups, the rats in the treatment group received 100 micromol/L U0126 treatment at the dose of 10 micro, and dimethyl sulfoxide (DMSO) were given in the normal control and ALI groups. Arterial blood gas and the extravascular lung water (EVLW) content were measured after the treatments, and pathological changes in the lung tissues were observed microscopically. ATII cells were isolated from the lung tissues and identified using tannic acid staining and alkaline phosphatase (APK) staining. The expression of AQP-4 mRNA in the cells was detected with RT-PCR. RESULTS: Blood gas analysis, HE staining and EVLW content measurement revealed severer injury of the lung tissues in ALI group than in the normal control group, but the severity was comparable between the treatment and ALI groups. RT-PCR demonstrated significantly increased AQP-4 mRNA expression in ALI group as compared with that in the normal control group, and U0126 treatment resulted in obvious reduction in AQP-4 mRNA expression in the U0126 treatment group. CONCLUSION: Oleic acid-induced ALI results in the activation of MAPK signaling pathway and up-regulation of AQP-4 mRNA expression in the ATII cells of rats.
OBJECTIVE: To investigate the relationship between aquaporin 4 (AQP4) in alveolar type II (AT-II) cells and MAPK signaling pathway in rats with early-stage oleic acid-induced acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). METHODS: Three groups of rats, namely the normal control, ALI and U0126 treatment group were used in this study. After oleic acid-induced ALI in the latter two groups, the rats in the treatment group received 100 micromol/L U0126 treatment at the dose of 10 micro, and dimethyl sulfoxide (DMSO) were given in the normal control and ALI groups. Arterial blood gas and the extravascular lung water (EVLW) content were measured after the treatments, and pathological changes in the lung tissues were observed microscopically. ATII cells were isolated from the lung tissues and identified using tannic acid staining and alkaline phosphatase (APK) staining. The expression of AQP-4 mRNA in the cells was detected with RT-PCR. RESULTS: Blood gas analysis, HE staining and EVLW content measurement revealed severer injury of the lung tissues in ALI group than in the normal control group, but the severity was comparable between the treatment and ALI groups. RT-PCR demonstrated significantly increased AQP-4 mRNA expression in ALI group as compared with that in the normal control group, and U0126 treatment resulted in obvious reduction in AQP-4 mRNA expression in the U0126 treatment group. CONCLUSION:Oleic acid-induced ALI results in the activation of MAPK signaling pathway and up-regulation of AQP-4 mRNA expression in the ATII cells of rats.