Abstract
Background/aim Currently, there is not any specific treatment for chronic pancreatitis (CP). It was aimed to investigate the effects of melatonin administration on endoplasmic reticulum (ER) stress, oxidative stress, fibrosis, biochemical and histopathological parameters, and Abcc2,Abcc5, and Abcg2 gene levels in an experimental rat CP model.Materials and methods Forty rats were randomized into five groups: Sham, CP, CP+25 mg/kg melatonin, CP+50 mg/kg melatonin, and CP+placebo. In all rats, except the sham group, a model of chronic pancreatitis was accomplished with intraperitoneal caerulein administration. In treatment groups, melatonin was used as a therapeutic agent. Serum TGF-β, TNF-α, MDA and GPx levels were studied. Pancreatic tissues were evaluated histopathologically. The expression levels of αSma,IR1α,Perk,Abcc2,Abcc5, and Abcg2 genes were measured with the qRT-PCR.Results Biochemical results of the melatonin groups exhibited favorable changes compared to the CP and placebo groups. α Sma,IR1α,Perk expression levels were significantly lower in the melatonin groups. The expression levels of Abcc2, Abcc5, and Abcg2 were significantly higher in the CP group compared to the sham group, and these gene levels were significantly lower in the melatonin groups compared to the CP group (p < 0.01, p < 0.05, p < 0.05, respectively).Conclusion In light of these favorable positive results, melatonin may be a useful preventive agent in the course of CP.
Highlights
Chronic pancreatitis (CP) is a disease characterized by progressive damage to the exocrine and endocrine parenchyma of the pancreas and is usually induced by alcohol and tobacco use [1]
Biochemical results of the melatonin groups exhibited favorable changes compared to the CP and placebo groups. αSma,IR1α,Perk expression levels were significantly lower in the melatonin groups
The expression levels of Abcc2, Abcc5, and Abcg2 were significantly higher in the CP group compared to the sham group, and these gene levels were significantly lower in the melatonin groups compared to the CP group (p < 0.01, p < 0.05, p < 0.05, respectively)
Summary
Chronic pancreatitis (CP) is a disease characterized by progressive damage to the exocrine and endocrine parenchyma of the pancreas and is usually induced by alcohol and tobacco use [1]. It reduces the patient quality of life, causes other systemic diseases and can lead to pancreatic cancer [2,3,4]. As with many chronic diseases, the mechanism of chronic pancreatitis is complex. Oxidative stress, impaired autophagy, ER stress, activation of proinflammatory cytokines, and increased apoptosis/necrosis have all been outlined in the pathogenesis of chronic pancreatitis.
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