SIRT6 ameliorates LPS-induced apoptosis and tight junction injury in ARDS through the ERK1/2 pathway and autophagy
Hanhan Liu, Sijiao Wang, Linjing Gong, Yue Shen, Fan Xu, Yali Wang, Lijuan Hu, Lei Zhu
Abstract
, the SIRT6-specific inhibitor OSS_128167 also significantly accelerated LPS-induced loss of tight junction proteins, lung inflammation, and apoptosis. Meanwhile, the SIRT6-specific inhibitor OSS_128167 also activated the ERK1/2 pathway and inhibited lung autophagy. These results suggested that SIRT6 could ameliorate the loss of tight junction proteins, inflammation, and apoptosis in LPS-induced ARDS by inhibiting the ERK1/ 2 pathway and enhancing autophagy, indicating that SIRT6 plays a beneficial role in ARDS and might be a potential therapeutic target for ARDS.
Topics & Concepts
AutophagyOccludinCell biologyGene knockdownApoptosisInflammationTight junctionCancer researchA549 cellSIRT6Small interfering RNAChemistryBiologyCell cultureImmunologyTransfectionSirtuinBiochemistryAcetylationGeneticsGeneHeme Oxygenase-1 and Carbon MonoxideNeuroinflammation and Neurodegeneration MechanismsAutophagy in Disease and Therapy