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NAD+ augmentation ameliorates acute pancreatitis through regulation of inflammasome signalling

by Khadka, Dipendra , Kwak, Sung Chul , Kim, Hyung-Jin , Lee, Seung Hoon , So, Hong-Seob , Shen, AiHua , Yang, Sei-Hoon , Kim, Hail , Pandit, Arpana , Kim, Hyun-Seok , Choe, Seong-Kyu , Cho, Eun-Young , Kwak, Tae Hwan , Oh, Gi-Su , Lee, Su-Bin , Park, Raekil

in 13/89 / 38/109 / 631/250/1933 / 631/80/86 / 64/110 / 82/51 / 96/1 / 96/106 / 96/63 / 96/95 / Adenine / Animals / Cell death / Ceruletide - toxicity / Homeostasis / Humanities and Social Sciences / Inflammasomes / Inflammasomes - metabolism / Inflammation / Lapachone / Mice, Inbred C57BL / MicroRNAs - metabolism / miRNA / multidisciplinary / NAD / NAD - metabolism / NAD(P)H Dehydrogenase (Quinone) - metabolism / Nicotinamide / p53 Protein / Pancreas / Pancreatitis / Pancreatitis, Acute Necrotizing - chemically induced / Pancreatitis, Acute Necrotizing - pathology / Science / Science (multidisciplinary) / Signal Transduction / SIRT1 protein / Sirtuin 1 - metabolism / TLR4 protein / Toll-like receptors / Tumor Suppressor Protein p53 - metabolism

2017

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2017

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2017

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Journal Article

NAD+ augmentation ameliorates acute pancreatitis through regulation of inflammasome signalling

Khadka, Dipendra,

Kwak, Sung Chul,

Kim, Hyung-Jin,

Lee, Seung Hoon,

So, Hong-Seob,

Shen, AiHua,

Yang, Sei-Hoon,

Kim, Hail,

Pandit, Arpana,

Kim, Hyun-Seok,

Choe, Seong-Kyu,

Cho, Eun-Young,

Kwak, Tae Hwan,

Oh, Gi-Su,

Lee, Su-Bin,

Park, Raekil

2017

Overview

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.

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Publisher

Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio

Subject

13/89

/ 38/109

/ 631/250/1933

/ 631/80/86

/ 64/110

/ 82/51

/ 96/1