Abstract

Oxidative stress plays an important role in the pathogenesis of acute pancreatitis. The exact pathogenesis of pancreatitis remains unknown but several mechanisms related to oxidative and inflammatory stress are implicated. It is reasonable to surmise that antioxidants would play a protective role in ameliorating the deleterious effects of pancreatitis. We have a wealth of data from animal models that reveal a positive correlation between antioxidant drugs and improved outcomes in experimental pancreatitis. Human clinical trials with antioxidants however, have disclosed conflicting results. We review the existing pathogenesis of pancreatitis related to oxidative stress and provide of a review of current trials with antioxidant therapy.

Highlights

  • Pancreatitis is a complex disorder the exact mechanism of which remains controversial

  • In a randomized placebo-controlled trial from China investigators examined the effect of intravenously-administered ascorbic acid delivered in patients with acute pancreatitis

  • The findings suggested that high endogenous serum levels of melatonin in the first 24 hours after the onset of acute pancreatitis (AP) correlated with a milder course of the disease, especially in younger patients [45]

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Summary

Introduction

Pancreatitis is a complex disorder the exact mechanism of which remains controversial. Oxidative metabolism of alcohol has been shown to produce ROS [25,26] and inhibit secretion from pancreatic acinar cells, events that trigger oxidative stress and inflammation through activation of NF-κB, and formation of TNF-α, IL-6, and other inflammatory mediators. Several studies by Jha et al in China have examined the effects of a naturally occurring Nrf2-keap1 pathway activator , resveratrol, on a rodent model of severe AP induced by sodium taurocholate [33,34,35,36,37,38].

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Conclusion

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