Abstract：
:Acute pancreatitis (AP) is a complicated disease without specific drug therapy. The cofactor nicotinamide adenine dinucleotide (NAD+) is an important regulator of cellular metabolism and homeostasis. However, it remains unclear whether modulation of NAD+ levels has an impact on caerulein-induced AP. Therefore, in this study, we investigated the effect of increased cellular NAD+ levels on caerulein-induced AP. We demonstrated for the first time that the activities and expression of SIRT1 were suppressed by reduction of intracellular NAD+ levels and the p53-microRNA-34a pathway in caerulein-induced AP. Moreover, we confirmed that the increase of cellular NAD+ by NQO1 enzymatic action using the substrate β-Lapachone suppressed caerulein-induced AP with down-regulating TLR4-mediated inflammasome signalling, and thereby reducing the inflammatory responses and pancreatic cell death. These results suggest that pharmacological stimulation of NQO1 could be a promising therapeutic strategy to protect against pathological tissue damage in AP.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Shen A,Kim HJ,Oh GS,Lee SB,Lee SH,Pandit A,Khadka D,Choe SK,Kwak SC,Yang SH,Cho EY,Kim HS,Kim H,Park R,Kwak TH,So HSdoi
10.1038/s41598-017-03418-0subject
Has Abstractpub_date
2017-06-07 00:00:00pages
3006issue
1issn
2045-2322pii
10.1038/s41598-017-03418-0journal_volume
7pub_type
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