To investigate the effect and mechanism of SIRT1 on inflammation in acute respiratory distress syndrome (ARDS) mice induced by lipopolysaccharide(LPS) .

The differences of related gene expression of lung tissues in two mice, including the SIRT1^{+ /-} mice with SIRT1 gene is knocked down and the wild-type mice, were detected by qRT-PCR and Western Blot. Then the ARDS model was induced in two kinds of mice by intraperitoneal injection of LPS, and the control group were injected with equal volume of saline. The pathological changes of lung tissue were observed by HE staining and the lung W/D ratio were calculated, the total protein concentration in BALF were detected by BCA, the levels of inflammatory factor tumour necrosis factor-α(TNF-α) and interleukin-6(IL-6) in bronchoalveolar lavage fluid (BALF) and plasma were tested by ELISA, the expression of p38 MAPK, p-p38 MAPK and p-ATF2 in lung tissue were detected by Western Blot.

Compared with wild-type mice, the mRNA and protein expression of SIRT1 in lung tissue in SIRT1^{+ /-} were significantly decreased, The difference was statistically significant(P<0.01). After ARDS induced by LPS, The pathological observation about two kinds of mice both showed infiltration of inflammatory cells in lung tissue, destruction of alveolar structure, edema of interstitial, thickening of alveolar septum, and SIRT1^{+ /-} mice were more severely damaged than wild-type mice. In SIRT1^{+ /-} mice, lung W/D ratio, total protein concentration in BALF, the levels of inflammatory factors TNF-α and IL-6 in BALF and plasma were significantly increased(P<0.05), the expression of p-p38 MAPK/p38 MAPK and p-ATF2 in lung tissues were increased more significantly than in wild-type mice(P<0.05).

The SIRT1 gene plays an important role in the inflammatory process of mice with ARDS induced by LPS, which may be related to the increased activity of p38 MAPK-p-ATF2 signaling pathway.