Sa1792 Development of a New Mouse Model of Chronic Pancreatitis Induced by Administration of L-Arginine

Garg, Sushil Kumar; Dawra, Rajinder; Barlass, Usman; Yuan, Zhihang; Dixit, Ajay Kumar; Saluja, Ashok

doi:10.1016/s0016-5085(14)61062-3

Cited by 2 publications

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“…In mice, this L-arginine-induced CP mimics features of human CP including pancreatic atrophy, fibrosis, inflammation, exocrine insufficiency and loss of architecture. 19 In this study, we induced Kunming and C57BL/6 mouse models with CP using L-arginine and caerulein, respectively, and treated the mice with ASA, aiming to explore the role of ASA in the progression of CP, and to identify a potential mechanism.…”

Section: Introductionmentioning

confidence: 99%

Aspirin Ameliorates Pancreatic Inflammation and Fibrosis by Inhibiting COX-2 Expression in Experimental Chronic Pancreatitis

Xu¹,

Fan²,

Xin³

et al. 2022

JIR

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Aim Chronic pancreatitis (CP) is a complex and intractable disease mainly manifested as chronic inflammation and fibrosis. Aspirin(acetylsalicylic acid, ASA) has been reported to be used in the treatment of acute pancreatitis (AP), but its effectiveness on CP is unclear. This study aimed to investigate the therapeutic effects of ASA in CP mice. Methods A murine model of CP was induced by intraperitoneal injection with 20% L-arginine. After one week of L-arginine administration, mice in the ASA treatment group were administered aspirin (100mg/kg/d) by intragastric gavage. At two, four, and six weeks after the first injection of L-arginine, mice were euthanized and the pancreas was collected for histological and molecular analysis. A second model of CP (caeruelin-induced) was used as a validation experiment to test the effect of ASA. Results L-arginine-induced CP resulted in over-expression of the inflammatory enzyme cyclooxygenase (COX)-2. COX-2 expression decreased after ASA treatment. Pancreatic-injury inflammatory response (measured by changes in amylase, CK-19, F4/80, CD3, MCP-1, IL-6) and fibrosis degree (measured by expression of COL1A1, MMP-1 and TIMP-1) was reduce in ASA -treated mice model. The therapeutic effect of ASA was also observed in caeruelin-induced CP. Conclusion ASA has an ameliorating effect in murine models of CP through inhibition of pancreatic inflammation and fibrosis, which may be a promising option for clinical treatment.

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Section: Introductionmentioning

confidence: 99%