Expression and effect of NLRP3 inflammasome in acute lung injury induced by seawater

Abstract

Objective To investigate the expression and the role of NOD-like receptor thermal-protein domain related protein (NLRP3) in the lung tissues and its mediated inflammatory factors in the occurrence and development of acute lung injury (ALI). Methods 50 healthy male SD rats were randomly divided into 5 groups: the control group, the seawater inhalation 1 h group, the seawater inhalation 3 h group, the seawater inhalation 6 h group and the seawater inhalation 9 h group, with 10 rats in each group. The rat injury model was established by the transtracheal seawater slow infusion (3 ml/kg). The rat lung paraffin sections were made and the pathomorphology was observed by HE staining. The wet/dry weight ratio of the lung tissue was detected in rats. The expressions of IL-1β and IL-18 in lung tissues were detected by ELISA. The expressions of IL-β, IL-18 and NLRP3 mRNA in lung tissue were detected by RT-PCR. The expression of NLRP3 protein in lung tissue was detected by Western-blot. Results The rat model of acute lung injury induced by seawater inhalation was successfully replicated. The wet/dry weight ratio of the lung tissue was significantly higher compared with the control group. There was a large number of inflammatory cell infiltration, edema and interstitial thickening in the lung tissue. The ELISA has revealed that the levels of IL-1β and IL-18 in the serum of rats gradually increase over time, reaching the peak in 3-6 hours, and then the expression of inflammatory factors gradually decreases. Compared with the results of the control group, the difference was statistically significant (P<0.05). The RT-PCR has found that the expression of mRNA of IL-1β and IL-18 in lung tissues of rats were similar to the expression of IL-1β and IL-18 in lung tissues of rats. Compared with results of the control group, the difference was statistically significant (P<0.05). Western Blot and RT-PCR have been used to detect the transcription and translation of NLRP3 in lung homogenate. The findings indicate that the mRNA and protein in NLRP3 in lung tissues increase gradually over time with the stimulation of seawater inhalation, and the difference was statistically significant (P<0.05). Conclusion NLRP3 inflammasome mediated inflammatory response may be involved in the pathogenesis of acute lung injury and aggravate the degree of lung injury, which may be one of the pathogenesis of acute lung injury induced by seawater. However, its role needs further confirmation. Key words: Acute lung injury; Seawater; NLRP3 inflammasome