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      Sesamol attenuates oxidative stress-mediated experimental acute pancreatitis in rats.

      Human & Experimental Toxicology
      Acute Disease, Amylases, secretion, Animals, Antioxidants, administration & dosage, therapeutic use, Benzodioxoles, Cell Line, Tumor, Cell Survival, drug effects, Ceruletide, toxicity, Disease Models, Animal, Dose-Response Relationship, Drug, Lipid Peroxidation, Male, Mice, Oxidative Stress, Pancreatitis, chemically induced, enzymology, pathology, prevention & control, Phenols, Rats, Rats, Wistar

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          Abstract

          Acute pancreatitis is a potentially fatal disease with no known cure. The initial events in acute pancreatitis may occur within the acinar cells. We examined the effect of sesamol on (i) a cerulein-induced pancreatic acinar cancer cell line, AR42J, and (ii) cerulein-induced experimental acute pancreatitis in rats. Sesamol inhibited amylase activity and increased cell survival. It also inhibited medium lipid peroxidation and 8-hydroxydeoxyguanosine in AR42J cells compared with the cerulein-alone groups. In addition, in cerulein-treated rats, sesamol inhibited serum amylase and lipase levels, pancreatic edema, and lipid peroxidation, but it increased pancreatic glutathione and nitric oxide levels. Thus, we hypothesize that sesamol attenuates cerulein-induced experimental acute pancreatitis by inhibiting the pancreatic acinar cell death associated with oxidative stress in rats.

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