PTSD is associated with disturbed hepatic morphology and metabolism. Neuronal mitochondrial dysfunction is considered a subcellular determinant of PTSD, but a link between hepatic mitochondrial dysfunction and hepatic damage in PTSD has not been demonstrated. Thus, the effects of experimental PTSD on the livers of high anxiety (HA) and low anxiety (LA) rats were compared, and mitochondrial determinants underlying the difference in their hepatic damage were investigated. Rats were exposed to predator stress for 10 days. Then, 14 days post-stress, the rats were evaluated with an elevated plus maze and assigned to HA and LA groups according to their anxiety index. Experimental PTSD caused dystrophic changes in hepatocytes of HA rats and hepatocellular damage evident by increased plasma ALT and AST activities. Mitochondrial dysfunction was evident as a predominance of small-size mitochondria in HA rats, which was positively correlated with anxiety index, activities of plasma transaminases, hepatic lipids, and negatively correlated with hepatic glycogen. In contrast, LA rats had a predominance of medium-sized mitochondria. Thus, we show links between mitochondrial dysfunction, hepatic damage, and heightened anxiety in PTSD rats. These results will provide a foundation for future research on the role of hepatic dysfunction in PTSD pathogenesis.

Preeclampsia (PE) is one of the most dangerous complications of pregnancy, characterized by hypertension, proteinuria, and symptoms of multiple organ failure, which are detected de novo after 20 weeks of pregnancy. The renin–angiotensin–aldosterone system (RAAS) is one of the first to recognize pregnancy and is an important regulator of blood pressure. The placenta has its own RAAS, the role of which in the development of PE is not fully understood. In this work, for the first time, we characterized the expression of RAAS components and miRNAs controlling it in the placenta at various times of PE manifestation. The data obtained will allow the development of a new strategy in the future for the search for therapeutic agents for patients suffering from PE and cardiovascular diseases.

Stress-induced conditions are associated with impaired cerebral blood flow (CBF) and increased risk of dementia and stroke. However, these conditions do not develop in resilient humans and animals. Here the effects of predator stress (PS, cat urine scent, ten days) on CBF and mechanisms of CBF regulation were compared in PS-susceptible (PSs) and PS-resilient (PSr) rats. Fourteen days post-stress, the rats were segregated into PSs and PSr groups based on a behavior-related anxiety index (AI). CBF and its endothelium-dependent changes were measured in the parietal cortex by laser Doppler flowmetry. The major findings are: (1) PS susceptibility was associated with reduced basal CBF and endothelial dysfunction. In PSr rats, the basal CBF was higher, and endothelial dysfunction was attenuated. (2) CBF was inversely correlated with the AI of PS-exposed rats. (3) Endothelial dysfunction was associated with a decrease in eNOS mRNA in PSs rats compared to the PSr and control rats. (4) Brain dopamine was reduced in PSs rats and increased in PSr rats. (5) Plasma corticosterone of PSs was reduced compared to PSr and control rats. (6) A hypercoagulation state was present in PSs rats but not in PSr rats. Thus, potential stress resilience mechanisms that are protective for CBF were identified.

Gestational diabetes mellitus (GDM) and preeclampsia (PE) are common pregnancy complications with similar risk factors. Although GDM is associated with PE, the exact mechanism underlying the association is unclear. The objective of this work was to study the morphofunctional and molecular changes in the placenta and peripheral blood in PE and GDM. Local and systemic changes in the production of several placental proteins were assessed along with markers of inflammation and metabolic disorders. Expression of placental lactogen, trophoblastic β1-glycoprotein, placental alpha-1-microglobulin, and proteinase 3 in villi was found to change in complicated pregnancy groups. Similarity of underlying pathogenic mechanisms was demonstrated for PE and GDM.

Преэклампсия (ПЭ) — специфичное для беременности мультисистемное воспалительное заболевание, характеризующееся развитием de novo артериальной гипертензии и протеинурии, а также полиорганной дисфункцией, представляющее угрозу для матери и плода. Патогенез ПЭ связан с системными дисфункциональными изменениями эндотелия сосудов и избыточной воспалительной реакцией матери, частично опосредованной освобождением плацентарного дебриса в материнскую циркуляцию, уровень депортации которого повышен при ПЭ. Кроме того, нарушение процессов ангиогенеза, инвазии трофобласта и ремоделирования спиральных артерий матки идентифицировано как ключевой фактор патогенеза ПЭ. Появляется все больше информации о возможном вовлечении в патогенез ПЭ нейтрофилов (НФ), которые в процессе активации формируют и высвобождают в межклеточное пространство нейтрофильные внеклеточные ловушки (neutrophil extracellular traps, NETs), предназначенные, главным образом, для элиминации патогенных микроорганизмов. Однако определенные условия, такие как конститутивная активация НФ, нарушение супрессорных механизмов и избыточная продукция NETs могут вносить вклад в патофизиологию ПЭ. Наряду с этим активированные НФ, по-видимому, играют важную роль как в усилении воспалительного ответа, так и в нарушении процесса свертывания крови и повышении риска тромбообразования. В настоящем обзоре представлены современные данные о биологиии NETs, механизме их формирования в зависимости от стимулов микроокружения, а также о потенциальной роли NETs в патогенезе ПЭ.

Mast cells (MCs) are highly differentiated and multifunctional immune cells. The importance of TC has been established not only as mediators of allergic reactions, but also for the development of an immune response, the occurrence of certain autoimmune diseases, tissue homeostasis, the formation of immunotolerance and metastasis of malignant tumors. MCs are present in the endometrium of women in various value depending on age, the phase of the menstrual cycle, the presence of pregnancy. Out of pregnancy, MCs are involved in the cyclic transformation of the uterine mucosa. At the onset of pregnancy, MCs stimulate the process of remodeling of the spiral arteries, the production of leukemia-inhibiting factor (LIF), which is the main implantation factor, and contribute to the formation of an immunotolerant state of the mother in relation to the fetus. Obstetric complications are accompanied by a variable content of MCs, which is associated with different genesis of diseases. A low amount of MCs is associated with impaired implantation and the development of early preeclampsia, an increased content of MCs is observed in the presence of a pathological inflammatory reaction that accompanies late preeclampsia. This review is devoted to the significance of MCs and their mediators in the physiological course of pregnancy, as well as their participation in the pathogenetic mechanisms of pregnancy complications.