Pharmacological stimulation of NQO1 decreases NADPH levels and ameliorates acute pancreatitis in mice.

ABSTRACT: Reactive oxygen species (ROS) regulates the activation of inflammatory cascades and tissue damage in acute pancreatitis. NADPH oxidase (NOX) is upregulated in pancreatitis and is one of the major enzymes involved in ROS production using NADPH as a general rate-limiting substrate. Dunnione, a well-known substrate of NAD(P)H:quinone oxidoreductase 1 (NQO1), reduces the ratio of cellular NADPH/NADP⁺ through the enzymatic action of NQO1. This study assessed whether a reduction in cellular NADPH/NADP⁺ ratio can be used to regulate caerulein-induced pancreatic damage associated with NOX-induced ROS production in animal models. Dunnione treatment significantly reduced the cellular NADPH/NADP⁺ ratio and NOX activity through the enzymatic action of NQO1 in the pancr

SUBMITTER: Shen A 

PROVIDER: S-EPMC6315021 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature