Platelet-rich plasma mitigates lipopolysaccharide-driven acute lung injury by targeting the cGAS-induced STING/ERS/TBK1/IRF3/NF-κB pathway in male rats.

One of the most frequent reasons behind respiratory failure is acute lung injury (ALI). In response to endoplasmic reticulum stress (ERS), the protein known as stimulator of interferon genes (STING) triggers strong lung inflammatory reactions and damage. The current study evaluated the possible influence of platelet-rich plasma (PRP) on ALI through altering the cyclic GMP-AMP synthase (cGAS)-triggered STING/ERS/TANK-binding kinase 1 (TBK1)/interferon regulatory factor 3 (IRF3)/nuclear factor kappa B (NF-κB) pathway. Twenty-one adult male Wistar rats were arbitrarily divided into three sets of seven: (1) control (CTRL); (2) ALI, in which the rats were given intraperitoneal (i.p.) lipopolysaccharide (LPS) at 10 mg/kg once; and (3) ALI + PRP, in which, at 1 week after i.p. LPS injection, rats were injected (i.p.) with PRP every 3 days for 4 weeks. At the end of the experiment, blood samples and lung tissues were evaluated at biochemical, molecular, and histological levels. PRP caused downregulation of the cGAS-induced STING/ERS/TBK1/IRF3/NF-κB signaling pathway and lessened lung inflammatory and apoptotic insults. This was evident on microscopic examination of lung tissue with significantly decreased immunoreactivity of lung tissue caspase 3, NF-κB, and tumor necrosis factor-alpha. PRP is a promising biological therapeutic regimen against ALI.