Protective Effect of Ertugliflozin against Acute Lung Injury Caused by Endotoxemia Model in Mice

Endotoxemic shock is characterized by multiple organ dysfunction, acute Lung Injury, acute respiratory distress syndrome, and high mortality. This study aimed to investigate the protective effect of ertugliflozin against acute lung injury during endotoxemia.
Materials &

Twenty adult Swiss-albino male mice, 9–13 weeks old, weighing 20–35 g, were divided into four groups (n=5) at random: the sham group (laparotomy without Cecal Ligation Puncture, CLP), the sepsis group (CLP), the vehicle group (DMSO for one week), and the ertugliflozin group (20 mg/kg/day orally for one week before CLP). After 24 hours of CLP, the lung tissue was removed and used for histological analysis. The inflammatory cytokines, including IL-1β, IL-6, TNF-alpha, TLR4, MIF, oxidative stress marker, and 8-isoPGF2-alpha, were measured.

In sepsis group, lung tissue levels of IL-6, IL-1, TNF-, MIF, TLR4 and F2-isoprostane were substantially greater than those in the sham group. In comparison to the sepsis group, the ertugliflozin treated mice exhibited significantly lower levels of inflammatory cytokines. Histologically, all of the mice in the sepsis group had considerable lung tissue injury, but in the ertugliflozin pre-treated group, there was a significant reduction in lung tissue injury.

Ertugliflozin attenuates lung dysfunction during endotoxemia in male mice via downstream inflammatory and oxidative stress signaling pathways.