Physiology and Pharmacology Department, College of Medicine and King Khalid University Hospital, King Saud University, P.O. Box 2925, Riyadh, 11461, Saudi Arabia.
Pharmacology and Toxicology Department, College of Pharmacy, Zagazig University, Zagazig, Egypt.
Dig Dis Sci. 2020 Dec;65(12):3583-3591. doi: 10.1007/s10620-020-06072-1. Epub 2020 Feb 22.
Acute pancreatitis (AP) is a sudden inflammation of the pancreas that may be life-threatening disease with high mortality rates, particularly in the presence of systemic inflammatory response and multiple organ failure. Oxidative stress has been shown to be involved in the pathophysiology of acute pancreatitis.
This study is designed to investigate the possible effect of mesna on an experimental model of cerulein-induced acute pancreatitis.
Animals were divided into five groups: Group 1 served as a control group given the saline; group II (mesna group) received mesna at a dose of (100 mg/kg per dose, i.p.) four times; group III (acute pancreatitis group) received cerulein at a dose of (20 µg/kg/dose, s.c.) four times with 1-h intervals; group VI, cerulein + mesna, was treated with mesna at a dose of (100 mg/kg, i.p.) 15 min before each cerulein injection.
Animals with acute pancreatitis showed elevated serum amylase and lipase levels. Biochemical parameters showed increased pancreatic tumor necrosis factors-α (TNF-α) and interleukin-1β (IL-1β) levels. A disturbance in oxidative stress markers was evident by elevated pancreatic lipid peroxides (TBARS) and decline in pancreatic antioxidants' concentrations including reduced glutathione (GSH); superoxide dismutase (SOD); and glutathione peroxidase (GSH-Px). Histological examination confirmed pancreatic injury. Pre-treatment with mesna was able to abolish the changes in pancreatic enzymes, oxidative stress markers (TBARS, SOD, GSH and GSH-Px), pancreatic inflammatory markers (TNF-α, IL-1β) as well as histological changes.
Mesna mitigates AP by alleviating pancreatic oxidative stress damage and inhibiting inflammation.
急性胰腺炎(AP)是一种胰腺的突然炎症,可能是一种致命的疾病,死亡率很高,特别是在存在全身炎症反应和多器官衰竭的情况下。氧化应激已被证明与急性胰腺炎的病理生理学有关。
本研究旨在探讨美司钠对胆胰酶诱导的急性胰腺炎实验模型的可能影响。
动物分为五组:第 1 组为对照组,给予生理盐水;第 2 组(美司钠组)给予美司钠(100mg/kg/次,腹腔注射)4 次;第 3 组(急性胰腺炎组)给予 20µg/kg/次,皮下注射,间隔 1 小时,4 次;第 6 组,胆胰酶+美司钠,在每次胆胰酶注射前 15 分钟给予美司钠(100mg/kg,腹腔注射)。
急性胰腺炎动物血清淀粉酶和脂肪酶水平升高。生化参数显示胰腺肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)水平升高。氧化应激标志物的紊乱表现为胰腺脂质过氧化物(TBARS)升高和胰腺抗氧化剂浓度降低,包括还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)。组织学检查证实了胰腺损伤。美司钠预处理能消除胰腺酶、氧化应激标志物(TBARS、SOD、GSH 和 GSH-Px)、胰腺炎症标志物(TNF-α、IL-1β)以及组织学变化。
美司钠通过减轻胰腺氧化应激损伤和抑制炎症来缓解 AP。