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We studied the effect of acute emotional stress and exogenous IL-1β (5 μg/kg intraperitoneally) on the cytokine profi le of blood serum in Wistar rats with various behavioral characteristics in the open-fi eld test. Blood level of proinfl ammatory cytokine IL-1β decreased in behaviorally passive rats, but increased in active animals after simultaneous immobilization and electrocutaneous stimulation. These changes refl ect the opposite immune responses to a similar stress exposure in rats with different emotional reactivity. Poststress variations in the concentration of circulating IL-1β differed in rats receiving exogenous IL-1β. Blood cytokine concentration decreased in behaviorally active rats, but remained unchanged in passive animals that were exposed to immobilization and electrocutaneous stimulation after pretreatment with IL-1β. Emotional stress and injection of IL-1β had no effect on blood level of an anti-infl ammatory cytokine IL-4 in rats. Our results indicate that rats with various behavioral parameters are characterized by signifi cant differences in the cytokine profi le of blood serum under conditions of emotional stress and treatment with IL-1β. These data illustrate the specifi c functional features of immune mechanisms, which provide an individual resistance of rats to the same stress exposure.A large body of evidence indicates that psychoemotional stress is accompanied by impairment of immune functions in mammals [9]. Immune dysfunction contributes to individual predisposition to stress factors.The pathogenesis of immune dysfunction during emotional stress involves changes in the cytokine profi le. Cytokines are polypeptide transmitters of cellcell interaction playing a regulatory role in normal physiological functions and progression of the defense response to foreign factors and impairment of tissue integrity [1]. Much attention is paid to the superfa mily of IL-1. IL-1β plays a trigger role and induces the cascade of cytokine secretion in the organism. IL-1β is one of the transmitters of the acute phase of the stress response. This cytokine modulates functional activity of the hypothalamic-pituitary-adrenal axis [8]. Our previous studies demonstrated an antistress effect of IL-1β on rats. Intracerebroventricular injection of IL-1β to animals prevents gastric ulceration [3] and involution of the spleen [5] and modulates the oxidative status of the hypothalamus and sensorimotor cortex of the brain under conditions of water-immersion stress [4].

The effects of melatonin (epiphyseal neurohormone) on the serum cytokine profiles of rats with different behavioral characteristics were studied after acute emotional stress. One-hour immobilization of animals with simultaneous electrocutaneous stimulation of subthreshold intensity served as the stress model. Acute stress exposure of animals with active behavior led to reduction of the peripheral blood concentrations of pro-inflammatory (IL-1α, IL-1β, IL-2, IFN-γ, granulomonocytic CSF) and anti-inflammatory (IL-4, IL-10) cytokines. Passive rats exposed to emotional stress developed a pronounced increase of pro-inflammatory IL-1β concentration. Reduction of pro-inflammatory cytokine levels in active rats exposed to stress was less pronounced after intraperitoneal preinjection of melatonin (2 mg/kg). In passive animals, exogenous melatonin inverted the poststress changes in the serum levels of pro-inflammatory IL-2 cytokine and of anti-inflammatory IL-4 and IL-10 cytokines. The modulatory effect of melatonin on the cytokine profiles of rats with different behavioral parameters seemed to contribute to adaptation of animals to emotional stress exposure.

We studied the effect of a pro-inflammatory cytokine IL-1β (5 μg/kg intraperitoneally) on blood leukocytes in Wistar rats various behavioral characteristics during acute emotional stress (1-h immobilization with simultaneous delivery of subthreshold electrocutaneous stimulation). Stress exposure was accompanied by a decrease in the total number of peripheral blood leukocytes in rats. Active animals were characterized by the increase in neutrophil count during stress. The number of eosinophils in passive specimens was shown to decrease under these conditions. Emotional stress was followed by a decrease in the lymphocyte index (by Shaganin) of active rats and increase in the leukocyte intoxication index (according to Kalf-Kalif) of passive specimens. Stress-induced changes in leukocytes differed after pretreatment with IL-1β. The number of blood leukocytes increased in animals receiving a cytokine injection before stress exposure. Exogenous IL-1β inverted (in active rats) or prevented (in passive specimens) a change in the percentage of various types of blood leukocytes, which was found after stress exposure. These data contribute to the understanding of peripheral mechanisms for the involvement of immunomodulatory cytokines in the systemic organization of physiological functions in specimens with different prognostic resistance to a similar stress exposure.

ВВЕДЕНИЕЭмоциональный стресс и связанные с ним психосоматические заболевания являются одной из наиболее актуальных проблем современной медико-биологической науки. Следствием стресса являются сердечно-сосудистые болезни, формирование эрозивно-язвенных поражений желудка, иммунные и эндокринные нарушения, расстройства психической деятельности и другие патологические состояния. Широкий спектр нарушений различных физиологических функций при эмоциональных стрессорных нагрузках говорит о том, что это состояние является разветвлённой системной реакцией организма [1]. 394Биомедицинская химия, 2015 том 61, вып. 3, с. 394-399. УДК 612.018+612.821 ©Коллектив авторов ВОЗДЕЙСТВИЕ МЕЛАТОНИНА НА АКТИВНОСТЬ АНТИОКСИДАНТНЫХ ФЕРМЕНТОВ В ЭРИТРОЦИТАХ КРОВИ КРЫС ПРИ ОСТРОМ ЭМОЦИОНАЛЬНОМ СТРЕССЕ

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The aim of this study is to investigate time-related changes in substance P (SP), beta-endorphin (BE), and corticosterone (CORT) levels due to DSIP aftereffects in the control and stress rats. Experiments were carried out on male Wistar and August rats. The SP and BE immunoreactivity in the hypothalamus and plasma samples was determined radioimmunologically. Blood CORT level was determined radioimmunologically. The rats were stressed at nighttime in special cages and tied by tails to the back side of the cage. The stress experiments were repeated for 12 hours for 5 days. There were 6 groups: 1. control animals, 2. stress animals, 3. rats that received DSIP in a dose of 60 nmol/kg one hour before decapitation, 4. rats in which DSIP was injected 24 hour before decapitation, 5. stressed rats in which DSIP was injected one hour before decapitation during the 5th exposure to stress, 6. stressed rats to which DSIP was injected 12 hours before the 5th exposure to stress, i.e., 24 hours before decapitation. Our experiments showed that DSIP administration induced marked changes in SP, BE, and CORT levels in hypothalamus and blood plasma. This suggests that the long-term stress-coping effect of DSIP depends on considerable changes in the level of other oligopeptides and hormones induced by DSIP. Evidently, DSIP triggers these processes inducing a cascade of interrelated molecular reactions radically different in animals with different resistance to emotional stress. This cascade of sequential reactions is different in Wistar and August rats differing by their resistance to emotional stress. DSIP administration stimulates the mechanism of resistance in August rats to a lesser extent than in Wistar animals.

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