Etanercept’s Protective Effect Against Lung Inflammation Caused by Polymicrobial Sepsis Induced by CLP in Male Rats

Inflammation and oxidative stress are critical factors leading to sepsis-induced severe lung injury (ALI). This study investigates the regulatory effects of Etanercept (ENT) in an animal model of sepsis-induced ALI. We established a cecal ligation and puncture (CLP) model for ALI in adult rats under anesthesia. Sepsis amplifies pathological lung tissue damage, lung endothelial permeability, serum inflammatory factor production, and the number of inflammatory cells in bronchoalveolar lavage fluid. Furthermore, it enhances the expression of phosphorylated NF-\(\kappa\)B p65, reduces lung superoxide dismutase due to CLP, and elevates lung malondialdehyde levels due to LPS-induced inflammatory factor production. This cascade of events exacerbates the expression of several genes, including TNF-\(\alpha\) and cytokines. LPS-induced inflammatory factor production also enhances the formation of reactive oxygen species in mitochondria. In summary, our current research provides evidence that ENT acts as a novel regulator of inflammation in sepsis-induced ALI in rats. The control of oxidative stress and the modulation of the inflammatory response are two key underlying mechanisms for the effects of ENT.