Hydrogen sulphide exacerbates acute pancreatitis by over-activating autophagy via AMPK/mTOR pathway.

ABSTRACT: Previously, we have shown that hydrogen sulphide (H₂ S) might be pro-inflammatory during acute pancreatitis (AP) through inhibiting apoptosis and subsequently favouring a predominance of necrosis over apoptosis. In this study, we sought to investigate the detrimental effects of H₂ S during AP specifically with regard to its regulation on the impaired autophagy. The incubated levels of H₂ S were artificially intervened by an administration of sodium hydrosulphide (NaHS) or DL-propargylglycine (PAG) after AP induction. Accumulation of autophagic vacuoles and pre-mature activation of trypsinogen within acini, which indicate the impairment of autophagy during AP, were both exacerbated by treatment with NaHS but attenuated by treatment with PAG. The regulation t

SUBMITTER: Ji L 

PROVIDER: S-EPMC5134374 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature