Inhibition of NLRP9b attenuates acute lung injury through suppressing inflammation, apoptosis and oxidative stress in murine and cell models.

Inhibition of NLRP9b attenuates acute lung injury through suppressing inflammation, apoptosis and oxidative stress in murine and cell models. Biochem Biophys Res Commun. 2018 Apr 12;: Authors: Yanling Q, Xiaoning C, Fei B, Liyun F, Huizhong H, Daqing S Abstract Acute lung injury (ALI), known a severe disease along with high morbidity and mortality, is lacking of specific therapies. Inflammation, apoptosis and oxidative stress are critical pathologies that contribute to ALI. Recently, there is study indicated that NLRP9b, a NOD-like receptor (NLR) member, is critical in modulation of inflammatory response. However, the effects of NLRP9b on sepsis-associated ALI, and the underlying molecular mechanism have not been understood. In the present study, the wild type (WT) and NLRP9b-knockout (NLRP9b-/-) mice with C57B/L6 background were subjected to a cecal ligation and puncture (CLP) for ALI murine model establishment. The findings indicated that NLRP9b-/- improved the survival rate of CLP-induced ALI mice, and inhibited pulmonary histopathological alterations, inflammation, and apoptosis. NLRP9b-/- reduced the activation of inhibitor of κBα/nuclear factor kappa B (IκBα/NF-κB), apoptosis-associated speck-like protein containing a Caspase-recruitment domain (ASC)/Casapse-1 and Caspase-3/poly (ADP-ribose) polymerase (PARP) signaling pathways in CLP-challenged mice with ALI. In vitro, mouse epithelial cells (MLE-12) were incubated with l...
Source: Biochemical and Biophysical Research communications - Category: Biochemistry Authors: Tags: Biochem Biophys Res Commun Source Type: research