Neurochemical Journal最新文献

{"title":"Dynamics of Prolactin and Hormones of the Hypothalamic-Pituitary Thyroid Axis in Patients with Schizophrenia","authors":"L. N. Gorobets, A. V. Litvinov, V. S. Bulanov","doi":"10.1134/s1819712424010069","DOIUrl":"https://doi.org/10.1134/s1819712424010069","url":null,"abstract":"<p><b>Abstract</b>—In 70 examined patients, 34 with the first psychotic episode (FPE) and 36 with chronic schizophrenia (CS), we studied dynamics of the prolactin (PRL), thyroid-stimulating hormone (TSH), and free thyroxine (T₄) during olanzapine therapy. Background hyperprolactinemia (HP) was observed in 52.9% of patients with FPE, which had with mean values of 971.1 ± 420 mIU/L, and in 50% of patients with CS (mean prolactin values were 1131 ± 845.4 mIU/L). In 11.8% of patients with FPE and in 16.6% of patients with CS, the level of free T₄ was below the standard values (mean values: 7.5 ± 0.3 pmol/L and 8.0 ± 0.8 pmol/L, respectively). TSH parameters in patients with FPE were within the reference values. Elevated background levels of TSH in patients with CS were observed in 11.1% of cases (4.8 ± 0.7 mIU/mL). By 6–8 weeks, an increase in mean PRL values was observed in all patients. Fluctuations in thyroid hormone levels by the end of therapy were insignificant. Four variants of dynamic changes in PRL and hypothalamic-pituitary-thyroid (HPT) axis hormones in patients during olanzapine therapy were identified. The relationship between PRL and thyroid hormones is discussed. The data obtained dictate the need to study the characteristics of the ratio of the levels of these hormones before the start of antipsychotic therapy (AT) in order to detect hypothyroidism and HP early, as well as to prevent the development of these hormonal dysfunctions in the process of AT and confirm the need to assess the levels of PRL and HPT-axis hormones in patients with FPE and CS before the start of the appointment of AT.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"22 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141152502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and Safety of Alteplase Combined with Urinarykallid for Intravenous Thrombolysis on Acute Cerebral Infarction","authors":"Jiahui Shao, Linyi Bao, Xinchun Jin, Haimiao Jin, Yun Chen","doi":"10.1134/s1819712424010203","DOIUrl":"https://doi.org/10.1134/s1819712424010203","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>This study aimed to explore the efficacy and safety of alteplase combined with urinarykallid for the intravenous thrombolysis of patients with acute cerebral infarction. Patients (<i>n</i> = 125) who were admitted to our hospital were included and divided into Group A (<i>n</i> = 60) and Group B (<i>n</i> = 65). Patients in Group A were treated with alteplase for intravenous thrombolysis, based on which urinarykallid was administered to patients in Group B as a combination treatment. Compared to Group A, Group B was significantly lower in hs-CRP and TNF-α levels (<i>p</i> &lt; 0.001), total incidence of adverse reactions (<i>p</i> &lt; 0.05), and NIHSS score (<i>p</i> &lt; 0.001) and higher in IL-10 level (<i>p</i> &lt; 0.001), total effective rate (markedly effective + effective/total cases × 100%. Compared to the single administration of alteplase, the combination of alteplase and urinarykallid for the intravenous thrombolysis of patients with acute cerebral infarction can achieve better efficacy at a lower incidence of adverse reactions and play a more significant role in clinical treatment.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"34 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141152554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Immune Function Enhancement and Clinical Symptom Alleviation in Epilepsy Patients Post-Topiramate Administration","authors":"Yuxiang Liu, Xiaojing Liu, Xiaofeng Zhu","doi":"10.1134/s181971242401015x","DOIUrl":"https://doi.org/10.1134/s181971242401015x","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>This study aimed to explore the amelioration of immune function and clinical symptoms in epilepsy patients following the implementation of topiramate therapy. We retrospectively analyzed 90 epilepsy patients treated at our institution from September 2020 to July 2022, segregating them into two groups: the observation group (<i>n</i> = 50, administered with a combination of carbamazepine and topiramate), and the control group (<i>n</i> = 40, treated with carbamazepine alone). The study evaluated disparities in clinical outcomes, immune function modifications, epilepsy score variances, quality of life indices, and incidence of adverse reactions before and after treatment in both groups. The observation group demonstrated a total treatment efficacy rate of 94.00% (47/50), significantly exceeding that of the control group, which stood at 75.00% (30/40) (<i>P</i> &lt; 0.05). Pre-treatment epilepsy and QOLIE-31 scores showed no statistically meaningful difference between the two groups (<i>P</i> &gt; 0.05); however, post-treatment evaluation after 3 months indicated that the observation group had significantly lower epilepsy scores and notably higher QOLIE-31 scores (<i>P</i> &lt; 0.05). Although pre-treatment immune function indices (including CD3+, CD4+, and IgA levels) did not show a significant difference between the groups (<i>P</i> &gt; 0.05), post-treatment levels of CD3+ and CD4+ were markedly higher, and IgA levels were lower in the observation group (<i>P</i> &lt; 0.05). The observation group also exhibited a reduced overall incidence of adverse reactions (12.00%, 6/50), significantly lower than the control group (32.50%, 13/40) (<i>P</i> &lt; 0.05). The adjunctive use of topiramate with standard therapy can enhance the clinical efficacy in epilepsy patients, ameliorating immune function, augmenting the quality of life, and escalating treatment safety, thereby presenting substantial value for clinical application.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"27 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141152500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PKM2 Activator TEPP-46 Suppresses Inflammation, Apoptosis, and Oxidative Disordering of Amyloid-Beta Treated Human Neuroblastoma","authors":"Lingling Wang, Tao Wang, Xiaohui Zhao, Haibing Ren, Jingshi Li, Juan Yang","doi":"10.1134/s1819712424010240","DOIUrl":"https://doi.org/10.1134/s1819712424010240","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Beta-amyloid peptides (Aβ) are common risk factors associated with cognitive impairment, neuroinflammation, and apoptosis in Alzheimer’s disease (AD). The glycolytic enzyme PKM2 is an essential antioxidant intermediate by promoting glutathione (GSH) biosynthesis, shielding neurons against oxidative damage, and conferring neuroprotective effects. However, its role in AD has rarely been reported. This study aimed to explore the mechanism underlying PKM2 activation in an AD cell model via the PKM2 activator TEPP-46. Aβ administration in SH-SY5Y cells reduced cell viability while increasing inflammation, apoptosis, and oxidative disorder. PKM2 activity, rather than its expression, was reduced in the AD cell model. TEPP-46 administration could restore PKM2 activity, reverse the suppressive effect of Aβ on cell viability and proliferation, reduce the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), decrease Aβ-triggered cell apoptosis, and restore cellular oxidative stress. Furthermore, the effect of TEPP-46 on the AD cell model was confirmed by deactivating P62, reversing the Bax/Bcl-2 ratio, and activating the Nrf2/HO-1 pathway by western blotting. Additionally, colivelin, an Nrf2 antagonist, deactivates the Nrf2/HO-1 pathway and recovers oxidative stress. Colivelin administration could also offset the influence of TEPP-46 on Aβ-induced SH-SY5Y cell inflammation and apoptosis and viability.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"46 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141152511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morpho-Functional Study of Cardioactive Neurohormones and Some Other Neuropeptides in the Nervous and Cardiac Systems of Rats in Normal and Pathological Conditions","authors":"S. S. Abrahamyan, A. Csillag, Z. Kh. Paronyan, I. K. Sahakyan, N. V. Tumasyan, N. V. Kocharyan, M. Palkovits","doi":"10.1134/s1819712423040025","DOIUrl":"https://doi.org/10.1134/s1819712423040025","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>This review presents data from multilateral studies, aimed at determining the localization, release and the function of the cardioactive hormones found by acad. A. Galoyan and colleagues in the hypothalamic-pituitary system of the bovine brain. The isolated protein-carriers of the neurohormones K, C and G (PCK, PCC, PCG) have been found to differ from the protein-carrier of the vasopressin and oxytocin neurophysin. The coronary-dilating factors were also isolated from the bovine heart and medulla of the adrenal gland. Later, in various regions of the intact rat brain, PCG was immunohistochemically detected in the glial and nerve cells, as well as in the varicose nerve fibers and synaptosomes. In the intact rat heart, PCG was localized in the nerve fibers, as well as in the small catecholamine-containing SIF cells. Fourteen days after the unilateral vagotomy, aimed at clarifying the origin of PCG-IR in the heart, some PCG-Ir nerve fibers around the cardiomyocytes and the ganglion cells were detected mainly due to the preserved SIF cells and SCG sympathetic neurons containing PCG. PCG-immunonegative cardiac ganglion cells in both intact and colchicine-treated rats were excluded as a possible source of the external PCG-IR. Thus, PCG, together with the other neuropeptides studied by us (NPY, CGRP and VIP, SP, LENK) present in SIF cells, can be involved in the local regulatory mechanisms of the heart, thereby confirming the idea proposed by A. Galoyan regarding the “neurosecretion of the heart” and the literature data on the existence of the peptidergic system of the heart.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"4 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140886610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anomalies of Energy Metabolism in Schizophrenia and Possible Pathogenetically Targeted Therapeutic Approaches","authors":"I. S. Boksha, T. A. Prokhorova, O. K. Savushkina, E. B. Tereshkina, E. A. Vorobyeva, G. Sh. Burbaeva","doi":"10.1134/s1819712423040086","DOIUrl":"https://doi.org/10.1134/s1819712423040086","url":null,"abstract":"<p><b>Abstract</b>—Coordinated regulation of energy conversion processes in the brain maintains its highly productive work and efficient mental activity. Impairments of the brain energy metabolism are considered among pathogenetic factors in the schizophrenia origin, but presently it is difficult to say whether these impairments are primary and causative for the development of the disease or represent consequences of certain changes in the functioning of neurotransmitter and other neurochemical systems. This review discusses the main results of the energy metabolism research in schizophrenia–at various levels and using different approaches, as well as regards some attempts of influencing the energy processes in the brain as an adjunctive therapy in schizophrenia. To date, the efficacy of these therapeutic approaches has not been proven, this may be due to the paucity of studies and the lack of preliminary identification/stratification of patient subgroups to whom the energy metabolism-targeted therapy would be the most useful. Based on the data presented, one can conclude that an analysis is necessary of relationships between the psychopathological manifestations of schizophrenia and energy metabolism deviations for further identification of those patients to whom the use of mitochondrial modulators, mitoprotection, and other approaches may represent a promising method of adjunctive therapy.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"289 1 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139647471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hemorphins—a Family of Atypical Opioid Peptides","authors":"F. P. Sarukhanyan, O. V. Hunanyan, H. H. Zakaryan","doi":"10.1134/s1819712423040207","DOIUrl":"https://doi.org/10.1134/s1819712423040207","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Hemorphins are a family of endogenous atypical opioid peptides released during the sequential cleavage of hemoglobin β-chain. Hemorphins are widely distributed in the organism and are implicated in pathophysiology of several diseases, including diabetes, cancer, Alzheimer disease and others. These peptides were identified several decades ago and their diverse therapeutic effects have been revealed. However, the exact molecular mechanisms involved in synthesis, metabolism and therapeutic effect of hemorphins are not fully understood. In this review, the current knowledge of hemorphins, focusing on their biological activity and Ca²⁺/CaM/CN-signaling pathway, involved in mechanisms of hemophins action is briefly summarized. These peptides have been intensively investigated at the Institute of Biochemistry (Armenia), and fundamental results are thoroughly discussed in this review.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"5 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139647623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Central Effects of Peripherally Administered Immune Cells Modulated by an Original Anticonvulsant in Experimental Alcoholism","authors":"E. V. Markova, I. V. Savkin, E. V. Serenko, M. A. Knyazheva, Yu. A. Shevchenko","doi":"10.1134/s1819712423030121","DOIUrl":"https://doi.org/10.1134/s1819712423030121","url":null,"abstract":"<p><b>Abstract</b>—Disruption of neuroimmune regulatory relationships caused by a change in the functional phenotype of immune cells due to chronic ethanol intoxication is an essential link in the pathogenesis of alcoholism. The unidirectional influence of most psychoactive drugs on the cells of the nervous and immune systems allows one to consider immune cells as model objects for influencing intersystem functional relationships. Based upon our own priority data on the presence of immunomodulatory properties of the original anticonvulsant acting on the molecular targets of ethanol in the central nervous system and the immune system in chronic alcohol intoxication, the aim of the present study was to evaluate the central effects of peripherally injected lymphocytes with the in vitro modulated functional activity by a synthetic ligand of the GABAA-receptor complex <i>meta</i>-chlorobenzhydrylurea in long-term alcoholized animals. It was shown that transplantation of lymphocytes precultured with the anticonvulsant in syngeneic long-term alcoholic recipients achieves a decrease in alcohol motivation and stimulation of behavioral activity in the “open field” test. Editing of behavioral patterns characteristic of chronic alcohol intoxication was recorded against the background of a decrease in proinflammatory cytokines IL-1β, IL-6, TNF-α, and IFN-γ and an increase in the anti-inflammatory cytokine IL-10 in pathogenetically significant brain structures, as well as an increase in the level of BDNF in the hippocampus, which allows us to consider a decrease in neuroinflammation and stimulation neuroplasticity as possible mechanisms for modification of the behavior of recipients. Visualization of functionally active lymphocytes precultured with <i>meta</i>-chlorobenzhydrylurea in the brain parenchyma of long-term alcoholized recipients also suggests a direct effect of injected lymphocytes on CNS cells. Thus, immune cells modulated in vitro with <i>meta</i>-chlorobenzhydrylurea by relatively independent mechanisms have positive psychoneuromodulating effects in chronic ethanol intoxication, which makes it possible to consider adoptive immunotherapy as a promising method in the treatment of alcoholism.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"22 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139647791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis in the Pathogenesis of Alzheimer’s Disease: The New Evidence for Validation of FAB Model","authors":"M. I. Aghajanov, H. S. Harutyunyan, A. Kh. Khamperyan, G. A. Karapetyan, K. S. Fereshetyan, K. B. Yenkoyan","doi":"10.1134/s1819712423040049","DOIUrl":"https://doi.org/10.1134/s1819712423040049","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Alzheimer’s disease is an age-associated progressive disorder, characterized by neurodegeneration and following cognitive decline. Several pathological alterations are implicated in its pathogenesis, hence etiology is still poorly understood. Ferroptosis is an alternative form of cell death, driven by intracellular accumulation of iron with subsequent reactive oxygen species formation, which damages membranes, proteins, and DNA, causing cell death. The imbalance in iron homeostasis is rapidly gaining weight as a neurodegeneration cause, increasing the need to develop in vivo and in vitro models to understand the role of ferroptosis in Alzheimer’s disease pathogenesis. This review focuses on the mechanisms of ferroptosis in the pathogenesis of AD, giving a detailed overview of the available in vivo and in vitro methods and their applications, as well as describing in detail the ferrous amyloid buthionine (FAB) model.</p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"107 4 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139647625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calpain Mediated Neurodegeneration in Parkinson’s disease","authors":"V. H. Knaryan","doi":"10.1134/s1819712423040116","DOIUrl":"https://doi.org/10.1134/s1819712423040116","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p> Parkinson’s disease (PD), a neurodegenerative movement disorder, is clinically manifested by disturbances in motor functions and non-motor symptoms, caused by progressive degeneration of nigrostriatal dopaminergic neurons and neurons in selected areas of the central and peripheral nervous system. The multifaceted pathogenesis of PD is associated with sustained mitochondrial dysfunction, oxidative stress, aberrant Са²⁺ homeostasis, which contribute to the activation of Са²⁺-dependent protease calpain. Calpain plays role in neuronal signaling mechanisms, ensuring the normal course of intracellular neurochemical and neurophysiological processes. In neuropathological conditions, elevation of intracellular Ca²⁺ and calpain activation, downregulation of endogenous and/or absence of exogenous pharmacological inhibitors of calpain, instigate calpain-mediated activation of apoptotic pathways, leading to degeneration and loss of selectively vulnerable nigrostriatal dopaminergic neurons in the brain. We have shown that at experimental (in vivo, in vitro) and human (<i>postmortem</i>) PD dorsal neurons and ventral motoneurons of the spinal cord are also affected through the calpain-mediated mechanisms of neurodegeneration. Synthetic calpain inhibitors – calpeptin, SNJ1945, and SJA6017, exhibited neuroprotective effects in the brain and spinal cord (in vivo, in vitro), suggesting calpain as a prospective target molecule for pharmacological therapy in the brain and spinal cord at PD<i>.</i></p>","PeriodicalId":19119,"journal":{"name":"Neurochemical Journal","volume":"26 1","pages":""},"PeriodicalIF":0.5,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139647489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}