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. 452* -адресат для переписки
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.
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