1Федеральное Государственное бюджетное учреждение "Научно-исследовательский институт общей патологии и патофизиологии" Российской академии медицинских наук, Москва 2 Федеральное Государственное бюджетное учреждение "Национальный Научный центр наркологии" Министерства здравоохранения РФ, 119002, Москва, Мал. Могильцевский пер., 3; тел.: +7 499 2419446; факс: +7 499 2419590; эл. почта: boris.davidov2@yandex.ru 3 Федеральное Государственное бюджетное образовательное учреждение высшего профессионального образования "Российский университет дружбы народов" РУДН, Москва У 37 пациентов с алкогольной болезнью печени (АБП) в плазме крови исследовано состояние окислительного стресса (ОС) при поступлении и через 2 недели от начала лечения. Пациенты были разделены на 3 группы алкогольный гепатит (АГ), алкогольный цирроз печени декомпенсированный (группа С по Чайлд-Пью) и пациенты в терминальной стадии (впоследствие умершие). У всех пациентов наблюдалось достоверное увеличение в плазме крови продуктов перекисного окисления липидов (диеновых конъюгатов и малонового диальдегида) и снижение уровня церулоплазмина. Коэффициент К ОС существенно превышал значения нормы как при поступлении, так и после проведения двухнедельного курса стандартного лечения, что указывает на важную роль ОС при АБП.Ключевые слова: активные формы кислорода, окислительный стресс, алкогольная болезнь печени, перекисное окисление липидов, антиоксидантная система.
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Chronic alcohol consumption is characterized by disturbances of neuroplasticity. Brain-derived neurotrophic factor (BDNF) is believed to be critically involved in this process. Here we aimed to review actual experimental and clinical data related to BDNF participation in neuroplasticity in the context of alcohol dependence. As has been shown in experiments with rodents, alcohol consumption is accompanied by the brain region-specific changes of BDNF expression and by structural and behavioral impairments. BDNF reverses aberrant neuroplasticity observed during alcohol intoxication. According to the clinical data parameters associated with BDNF demonstrate close correlation with neuroplastic changes accompanying alcohol dependence. In particular, the rs6265 polymorphism within the BDNF gene is associated with macrostructural changes in the brain, while peripheral BDNF concentration may be associated with anxiety, depression, and cognitive impairment. Thus, BDNF is involved in the mechanisms of alcohol-induced changes of neuroplasticity, and polymorphisms within the BDNF gene and peripheral BDNF concentration may serve as biomarkers, diagnostic or prognostic factors in treatment of alcohol abuse.
Some BDNF (brain-derived neurotrophic factor)-targeted microRNAs such as miR-30a-5p associate with alcohol dependence phenomenon however their relationship with AWS is not described. We aimed to measure serum BDNF concentration and relative content of miR-30a-5p over the course of alcohol abstinence and compare obtained results with clinics of AWS. Additionally, we studied relative serum content of miR-30a-5p, a microRNA which does not target BDNF but relates to alcohol use disorder. Serum BDNF concentration increased over the course of alcohol abstinence, contrary relative content of miR-122 but not miR-30a-5p decreased. Moreover, during AWS miR-122 but miR-30a-5p negatively correlated with serum BDNF concentrations. Relative content of miR-122 negatively correlated with depression and state anxiety levels on 8th day of abstinence. According to multiple regressions on 21st day of abstinence alcohol craving and cognitive disturbances may be predictors of serum BDNF concentration, and vice versa. Thus, serum BDNF concentration and relative content of miR-122 associate with some aspects of AWS clinics and may dynamically reflect AWS severity.
We proposed a new indicator for evaluation of functional activity of Ca(2+) in human blood serum based on lysis of sheep erythrocytes with 10% human blood serum in the presence of 0.55 mM ethylene glycol tetraacetic acid at 37°C for 10 min. After incubation, the degree of sheep erythrocytes lysis inhibition is estimated: inhibition of complement hemolytic activity <30% is considered as high functional Са(2+) activity, inhibition by 31-70% corresponds to normal activity, and >71% indicates low activity. The comparative studies of complement activating function of heterophilic antibodies, complement system reactivity in the presence of 0.29 M NaCl, and functional activity of ionized Ca(2+) make possible estimation of the individual's immune status.
Morphine injected subcutaneously in a dose of 2 mg/kg body weight exerted an analgesic effect in some Wistar rats (morphine-sensitive animals), as was indicated by a significantly prolonged latency of the tail-flick response, but failed to produce analgesia in others (morphine-insensitive animals). In morphine-sensitive rats, the striatum had the highest enkephalinase A activity, followed in decreasing order by the mesencephalon, hippocampus, pons, cortex, medulla oblongata, and hypothalamus. Thirty minutes after intraperitoneal administration of naloxone (0.3 mg/kg body weight) to morphine-sensitive rats, enkephalinase activity fell significantly in the hippocampus, striatum, and cortex, remained unchanged in the pons and medulla oblongata, and rose significantly in the meseneephalon and insignificantly in the hypothalamus; generally similar differences in enkephalinase activity from naloxone-untreated morphine-sensitive rats were recorded in the brain structures of morphine-insensitive rats given saline instead of naloxone.
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