Вплив меланіну на ферментативну активність підшлункової залози в умовах гострого стресу

Abstract

На експериментальній моделі гострого стресу доведена цитопротекторна роль меланіну на підшлункову залозу. Встановлено, що за умов гострого стресу в підшлунковій залозі тварин стресонестійкого типу виникає протеїназно-інгібіторний дисбаланс, про що свідчить вірогідне зростання загальної протеолітичної активності на тлі зменшення інгібіторів протеїназ та підвищення активності ферментів цитолітичного синдрому: амілази і ліпази. Попереднє введення меланіну стресованим щурам сприяло нормалізації протеіназно-інгібіторного потенціалу та попереджало розвиток цитолізу підшлункової залози.

На экспериментальной модели острого стресса доказана цитопротекторная роль меланина на поджелудочную железу крыс. Установлено, что острый стресс вызывает в поджелудочной железе стрессонеустойчивых животных протеиназно-ингибиторный дисбаланс, о чем свидетельствует достоверное повышение общей протеолитической активности на фоне снижения ингибиторов протеиназ и повышение ферментов цитолитического синдрома: амилазы и липазы. Введение меланина стрессированным животным способствовало нормализации протеиназно-ингибиторного потенциала и предупреждало развитие цитолитического синдрома поджелудочной железы.

Currently, society living in the “western” way has faced the increase in prevalence of lifestyle diseases which share psychological stress as common pathophysiological basis. Chronic adverse effects experienced by humans in conditions of anthropogenic pressing, social instability, and intense rhythm of life can be both the main and additional etiological factor for many diseases. One of the consequences of stress factors is the activation of cytolysis and change of enzyme activity of the pancreas. In particular, the activation of pancreatic proteases induces the degeneration (autolysis) of pancreas, acute pancreatitis as well as the damage of nearby organs. Previously, some reports demonstrated convincingly that pancreas as a main source of aggressive hydrolyses played an important role in tissue damage during the catabolic phase of stress syndrome. Thus, our study is aimed to investigate differences of pancreatic enzyme activity depending on individual and typological characteristics and melanin stress-protecting properties in the pancreas of rats. The study involved 84 Wistar malerats weighing 180-220 g. All manipulations on animals were carried out in accordance with “European convention for the protection of vertebrate animals used for experimental and other scientific purposes” (Strasbourg, 1986). To simulate acute immobilization stress the animals were fixed lying on the back as long as 3 hrs. Stress resistance of the animals was determined by means of open-field test and variable data obtained. The test animals, which showed rapid adaptation, low indicators of motor activity, exploratory behavior, and vegetative balance were rated as stress-resistant ones, while the rats with low adaptation, high parameters of motor activity, exploratory behavior, and vegetative balance were described as a stress-susceptible group. The control group was made up of the animals of the respective type. The rats were sacrificed by phlebotomy carried out under hexenal anesthesia (50 mg/kg). The pancreas of the animals was the object of research to investigate the total proteolytic, antitrypsic, amylase (EC: 3.2.1.1) and lypolytic activity (EC: 3.1.1.3). 30 minutes prior modeling acute stress the rats were administered synthetic melanin (Sigma) in a dose of 5 mg/kg intragastrically. The obtained data were processed with generally acceptedmethod of variation statistics.Thus, under the conditions of acute stress the development of protease inhibitors imbalance as well as an increase in amylase and lipase activity is evident. Prior administration of melanin against the acute stress results in a decrease in the activity of proteases, amylase, lipase, and the increase in the total antitryptic activity that vindicates stress-protective action produced by melanin upon the pancreas.