2. Academic Validation
  3. DPP4 Inhibitor Attenuates Severe Acute Pancreatitis-Associated Intestinal Inflammation via Nrf2 Signaling

DPP4 Inhibitor Attenuates Severe Acute Pancreatitis-Associated Intestinal Inflammation via Nrf2 Signaling

  • Oxid Med Cell Longev. 2019 Nov 15;2019:6181754. doi: 10.1155/2019/6181754.
Xiang Zhou 1,  Weiming Wang 1,  Cheng Wang 2,  Chenlei Zheng 1,  Xiangxiang Xu 1,  Xiaofeng Ni 1,  Shanshan Hu 1,  Binbin Cai 1,  Linxiao Sun 1,  Keqing Shi 1 2,  Bicheng Chen 1 2,  Mengtao Zhou 1 2,  Gang Chen 1 2
Affiliations

Affiliations

  • 1 Department of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000 Zhejiang Province, China.
  • 2 Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000 Zhejiang Province, China.
PMID: 31827684 DOI: 10.1155/2019/6181754
Abstract

Severe acute pancreatitis (SAP) is a challenging disease with high morbidity and mortality, often complicated by multiple organ dysfunction syndrome (MODS). The intestine, a major organ involved in MODS, correlates strongly with the evolution of the disease. In this study, we demonstrated that the DPP4 inhibitor, sitagliptin, protects SAP-associated intestinal injury both in vitro and in vivo. These beneficial effects were achieved by suppressing oxidative stress and inflammatory responses. Moreover, in sitagliptin-treated SAP mice, expression of Nrf2 was induced and that of NF-κB was reduced, compared to the control SAP mice. In addition, we used Nrf2-/- mice to test the protective effect of Nrf2 during sitagliptin treatment of SAP; our results indicated that Nrf2-/- mice had greater pancreatic and intestinal injury than wild-type mice. Taken together, high levels of ROS induced by SAP may be inhibited by sitagliptin, possibly by inactivating the Nrf2-NF-κB pathway.

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