Pharmacological reports : PR最新文献

{"title":"The impact of the histone deacetylase inhibitor sodium butyrate on microglial polarization after oxygen and glucose deprivation.","authors":"Karolina Ziabska,&nbsp;Justyna Gargas,&nbsp;Joanna Sypecka,&nbsp;Malgorzata Ziemka-Nalecz","doi":"10.1007/s43440-022-00384-x","DOIUrl":"https://doi.org/10.1007/s43440-022-00384-x","url":null,"abstract":"<p><strong>Background: </strong>Microglia play a major role in the development of brain inflammation after central nervous system injury. On the other hand, microglia also participate in the repair process. The dualistic role of these cells results from the fact that various states of their activation are associated with specific phenotypes. The M1 phenotype is responsible for the production of proinflammatory mediators, whereas the M2 microglia release anti-inflammatory and trophic factors and take part in immunosuppressive and neuroprotective processes. The histone deacetylase inhibitor sodium butyrate (SB) shows anti-inflammatory and neuroprotective effects in some animal models of brain injury. The aim of this study was to examine the effects of sodium butyrate on the proliferation and M1/M2 polarization of primary microglial cells after oxygen and glucose deprivation (OGD) in vitro.</p><p><strong>Methods: </strong>Primary microglial cultures were prepared from 1-day-old rats, subjected to the OGD procedure and treated with SB (0.1 mM, 1 mM and 10 mM). The effect of OGD and SB on microglial proliferation was assessed by double immunofluorescence, and microglial phenotypes were evaluated by qPCR.</p><p><strong>Results: </strong>The OGD procedure stimulated the proliferation of microglia after 24 h of culturing, and SB treatment reduced the division of these cells. This effect was inversely proportional to the SB concentration. The OGD procedure increased proinflammatory CD86 and IL1β gene expression and reduced the expression of the anti-inflammatory M2 markers arginase and CD200 in microglia.</p><p><strong>Conclusions: </strong>SB can change the polarization of microglia after OGD from an unfavourable M1 to a beneficial M2 phenotype. Our results show that SB is a potential immunosuppressive agent that can modulate microglial activation stimulated by ischaemic-like conditions.</p>","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"909-919"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40478082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Voltage-clamp evidence of GABA_A receptor subunit-specific effects: pharmacodynamic fingerprint of chlornordiazepam, the major active metabolite of mexazolam, as compared to alprazolam, bromazepam, and zolpidem.","authors":"Hélder Fernandes,&nbsp;Vânia Batalha,&nbsp;Ellen Braksator,&nbsp;Simon Hebeisen,&nbsp;Maria João Bonifácio,&nbsp;Maria Augusta Vieira-Coelho,&nbsp;Patrício Soares-da-Silva","doi":"10.1007/s43440-022-00411-x","DOIUrl":"https://doi.org/10.1007/s43440-022-00411-x","url":null,"abstract":"<p><strong>Background: </strong>Anxiolytic benzodiazepines, due to their clinical effectiveness, are one of the most prescribed drugs worldwide, despite being associated with sedative effects and impaired psychomotor and cognitive performance. Not every GABA_A receptor functions in the same manner. Those containing α1 subunits are associated with sleep regulation and have a greater effect on the sedative-hypnotic benzodiazepines, whereas those containing α2 and/or α3 subunits are associated with anxiety phenomena and have a greater effect on the anxiolytic benzodiazepines. Therefore, characterization of the selectivity profile of anxiolytic drugs could translate into a significant clinical impact.</p><p><strong>Methods: </strong>The present study pharmacodynamically evaluated chlornordiazepam, the main active metabolite of mexazolam, upon GABA_A receptors containing α2 and/or α3, anxiety-related, and those containing an α1 subunit, associated with sleep modulation.</p><p><strong>Results: </strong>As shown by whole-cell patch-clamp data, chlornordiazepam potentiated GABA-evoked current amplitude in α2 and α3 containing receptors without changing the current amplitude in α1 containing receptors. However, current decay time increased, particularly in GABA_A receptors containing α1 subunits. In contrast, other anxiolytic benzodiazepines such as alprazolam, bromazepam, and zolpidem, all increased currents associated with GABA_A receptors containing the α1 subunit.</p><p><strong>Conclusions: </strong>This novel evidence demonstrates that mexazolam (through its main metabolite chlornordiazepam) has a \"pharmacodynamic fingerprint\" that correlates better with an anxiolytic profile and fewer sedative effects, when compared to alprazolam, bromazepam and zolpidem, explaining clinical trial outcomes with these drugs. This also highlights the relevance of the pharmacological selectivity over GABA_A receptor subtypes in the selection of benzodiazepines, in addition to their clinical performance and pharmacokinetic characteristics.</p>","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"956-968"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33464419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk between neurological, cardiovascular, and lifestyle disorders: insulin and lipoproteins in the lead role.","authors":"Richa Tyagi,&nbsp;Bhupesh Vaidya,&nbsp;Shyam Sunder Sharma","doi":"10.1007/s43440-022-00417-5","DOIUrl":"https://doi.org/10.1007/s43440-022-00417-5","url":null,"abstract":"<p><p>Insulin resistance and impaired lipoprotein metabolism contribute to a plethora of metabolic and cardiovascular disorders. These alterations have been extensively linked with poor lifestyle choices, such as consumption of a high-fat diet, smoking, stress, and a redundant lifestyle. Moreover, these are also known to increase the co-morbidity of diseases like Type 2 diabetes mellitus and atherosclerosis. Under normal physiological conditions, insulin and lipoproteins exert a neuroprotective role in the central nervous system. However, the tripping of balance between the periphery and center may alter the normal functioning of the brain and lead to neurological disorders such as Alzheimer's disease, Parkinson's disease, stroke, depression, and multiple sclerosis. These neurological disorders are further characterized by certain behavioral and molecular changes that show consistent overlap with alteration in insulin and lipoprotein signaling pathways. Therefore, targeting these two mechanisms not only reveals a way to manage the co-morbidities associated with the circle of the metabolic, central nervous system, and cardiovascular disorders but also exclusively work as a disease-modifying therapy for neurological disorders. In this review, we summarize the role of insulin resistance and lipoproteins in the progression of various neurological conditions and discuss the therapeutic options currently in the clinical pipeline targeting these two mechanisms; in addition, challenges faced in designing these therapeutic approaches have also been touched upon briefly.</p>","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"790-817"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33479357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simultaneous determination of four antibiotics in human urine and hair samples employing a simple and efficient dispersive micro solid-phase extraction-high performance liquid chromatography.","authors":"Ehsan Soleimanirad,&nbsp;Anousheh Badameh,&nbsp;Arastou Raoufi,&nbsp;Mahmoud Ebrahimi","doi":"10.1007/s43440-022-00404-w","DOIUrl":"https://doi.org/10.1007/s43440-022-00404-w","url":null,"abstract":"<p><strong>Background: </strong>Antibiotics containing azithromycin, amoxicillin, doxycycline, tetracycline, and azithromycin are widely utilized in the treatment of bacterial infections, and their determination in biological samples is critical to evaluate their side effects.</p><p><strong>Methods: </strong>A dispersive micro solid-phase extraction (DMSPE) as an efficient sample preparation was developed for the simultaneous extraction of the antibiotics in biological samples. For this purpose, chitosan@Fe₃O₄ nanoparticles were prepared as a green and magnetic sorbent based on a chemical coating of Fe₃O₄ nanoparticles with chitosan.</p><p><strong>Results: </strong>The sorbent was compared with several sorbents such as ZnO NPs, CuO NPs, and Fe₃O₄ NPs to extract the antibiotics. In addition, effective factors for antibiotic extraction were evaluated and optimized using a central composite design and one factor at a time. The method has wide linearity in the concentration ranges of 2.1-800.0, 3.5-1000.0, 2.0-800.0, and 2.7-1000.0 μg L^-1 with an R-squared higher than 0.9958 for the determination of azithromycin, amoxicillin, doxycycline, and tetracycline, respectively. The limit of detection and limit of quantitation was lower than 1.1 and 3.5 μg L^-1, respectively. The relative standard deviations (RSDs) were also lower than 4.90% for the determination of the analytes at a concentration of 20.0 µg L^-1. High recoveries in the percentage range of 94.70-106.75%, with RSDs between 4.64 and 5.83%, were obtained to analyze spiked urine and hair samples.</p><p><strong>Conclusions: </strong>The DMSPE-HPLC-DAD procedure displayed various advantages for determining antibiotics, including simple operation, high recoveries, low sample solution and desorption solvent consumption, high preconcentration factors, proper determination time, and simple and inexpensive method of sorbent preparation.</p>","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"1069-1082"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33490291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interaction between moxifloxacin and Mcl-1 and MITF proteins: the effect on growth inhibition and apoptosis in MDA-MB-231 human triple-negative breast cancer cells.","authors":"Artur Beberok,&nbsp;Jakub Rok,&nbsp;Zuzanna Rzepka,&nbsp;Krzysztof Marciniec,&nbsp;Stanisław Boryczka,&nbsp;Dorota Wrześniok","doi":"10.1007/s43440-022-00407-7","DOIUrl":"https://doi.org/10.1007/s43440-022-00407-7","url":null,"abstract":"<p><strong>Background: </strong>Microphthalmia-associated transcription factor (MITF) activates the expression of genes involved in cellular proliferation, DNA replication, and repair, whereas Mcl-1 is a member of the Bcl-2 family of proteins that promotes cell survival by preventing apoptosis. The objective of the present study was to verify whether the interaction between moxifloxacin (MFLX), one of the fluoroquinolones, and MITF/Mcl-1 protein, could affect the viability, proliferation, and apoptosis in human breast cancer using both in silico and in vitro models.</p><p><strong>Methods: </strong>Molecular docking analysis (in silico), fluorescence image cytometry, and Western blot (in vitro) techniques were applied to assess the contribution of MITF and Mcl-1 proteins in the MFLX-induced anti-proliferative and pro-apoptotic effects on the MDA-MB-231 breast cancer cells.</p><p><strong>Results: </strong>We indicated the ability of MFLX to form complexes with MITF and Mcl-1 as well as the drug's capacity to affect the expression of the tested proteins. We also showed that MFLX decreased the viability and proliferation of MDA-MB-231 cells and induced apoptosis via the intrinsic death pathway. Moreover, the analysis of the cell cycle progression revealed that MFLX caused a block in the S and G2/M phases.</p><p><strong>Conclusions: </strong>We demonstrated for the first time that the observed effects of MFLX on MDA-MB-231 breast cancer cells (growth inhibition and apoptosis induction) could be related to the drug's ability to interact with MITF and Mcl-1 proteins. Furthermore, the presented results suggest that MITF and Mcl-1 proteins could be considered as the target in the therapy of breast cancer.</p>","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"1025-1040"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9585003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40333629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Selective cytotoxic and genotoxic activities of 5-(2-bromo-5- methoxybenzylidene)-thiazolidine-2,4-dione against NCI-H292 human lung carcinoma cells.","authors":"Maria do D Rodrigues,&nbsp;Priscila B G S Santiago,&nbsp;Karla M R Marques,&nbsp;Valéria R A Pereira,&nbsp;Maria C A B de Castro,&nbsp;Jeanne C L L Cantalice,&nbsp;Teresinha G da Silva,&nbsp;Mônica L Adam,&nbsp;Silene C do Nascimento,&nbsp;Julianna F C de Albuquerque,&nbsp;Gardenia C G Militao","doi":"10.1007/s43440-022-00376-x","DOIUrl":"https://doi.org/10.1007/s43440-022-00376-x","url":null,"abstract":"","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"1115"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40360405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2-Mercaptoethanol protects against DNA double-strand breaks after kidney ischemia and reperfusion injury through GPX4 upregulation.","authors":"Daeun Moon,&nbsp;Babu J Padanilam,&nbsp;Hee-Seong Jang,&nbsp;Jinu Kim","doi":"10.1007/s43440-022-00403-x","DOIUrl":"https://doi.org/10.1007/s43440-022-00403-x","url":null,"abstract":"<p><strong>Background: </strong>Kidney ischemia reperfusion injury (IRI) is characterized by tubular cell death. DNA double-strand breaks is one of the major sources of tubular cell death induced by IRI. 2-Mercaptoethanol (2-ME) is protective against DNA double-strand breaks derived from calf thymus and bovine embryo. Here, we sought to determine whether treatment with 2-ME attenuated DNA double-strand breaks, resulting in reduced kidney dysfunction and structural damage in IRI.</p><p><strong>Methods: </strong>Kidney IRI or sham-operation in mice was carried out. The mice were treated with 2-ME, Ras-selective lethal 3, or vehicle. Kidney function, tubular injury, DNA damage, antioxidant enzyme expression, and DNA damage response (DDR) kinases activation were assessed.</p><p><strong>Results: </strong>Treatment with 2-ME significantly attenuated kidney dysfunction, tubular injury, and DNA double-strand breaks after IRI. Among DDR kinases, IRI induced phosphorylation of ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3 related (ATR), but IRI reduced phosphorylation of other DDR kinases including ataxia telangiectasia and Rad3 related, checkpoint kinase 1 (Chk1), Chk2, and Chinese hamster cells 1 (XRCC1). Treatment with 2-ME enhanced phosphorylation of ATM and ATM-mediated effector kinases in IRI-subjected kidneys, suggesting that 2-ME activates ATM-mediated DDR signaling pathway. Furthermore, 2-ME dramatically upregulated glutathione peroxidase 4 (GPX4) in IRI-subjected kidneys. Inhibition of GPX4 augmented adverse IRI consequences including kidney dysfunction, tubular injury, DNA double-strand breaks, and inactivation of ATM-mediated DDR signaling pathway after IRI in 2-ME-treated kidneys.</p><p><strong>Conclusions: </strong>We have demonstrated that exogenous 2-ME protects against DNA double-strand breaks after kidney IRI through GPX4 upregulation and ATM activation.</p>","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"1041-1053"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40413008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential action of SSRIs in the treatment of skin diseases including atopic dermatitis and slow-healing wounds.","authors":"Aneta Kiecka,&nbsp;Marian Szczepanik","doi":"10.1007/s43440-022-00423-7","DOIUrl":"https://doi.org/10.1007/s43440-022-00423-7","url":null,"abstract":"<p><p>Selective serotonin reuptake inhibitors (SSRIs) are used to treat affective and anxiety disorders. Antidepressants have also been shown to have antimicrobial and immunomodulatory effects, which may affect the microbiota-intestinal-brain axis. Studies show that SSRIs have antimicrobial activity both in vivo and in vitro and influence bacteria by inhibiting biofilm, affecting efflux pumps, among others. A huge challenge today is the prevention and treatment of skin diseases, including atopic dermatitis (AD) and slow-healing wounds. Skin diseases including AD and non-healing wounds are serious medical problem. People suffering from these conditions feel constant discomfort, which also affects their psychological state. Research on new treatments for AD and slow-healing wounds is essential because current medications are not fully effective and have many side effects. Exploring new drug groups for AD and slow-healing wounds will allow for the creation of an alternative treatment for these diseases. SSRIs represent a hope for the treatment of skin diseases due to their immunomodulatory and antimicrobial properties.</p>","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"947-955"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9584846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33490292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of pharmacogenomic algorithm to optimize nateglinide dose for the treatment of type 2 diabetes mellitus.","authors":"Shaik Mohammad Naushad,&nbsp;Tajamul Hussain,&nbsp;Salman A Alrokayan,&nbsp;Vijay Kumar Kutala","doi":"10.1007/s43440-022-00400-0","DOIUrl":"https://doi.org/10.1007/s43440-022-00400-0","url":null,"abstract":"<p><strong>Background: </strong>Nateglinide is a meglitinide used for the treatment of type 2 diabetes mellitus. Individual studies demonstrated the association of CYP2C9, SLCO1B1, and MTNR1B variants with the safety and efficacy of nateglinide. The current study aimed to develop a pharmacogenomic algorithm to optimize nateglinide therapy.</p><p><strong>Methods: </strong>Multiple linear regression (MLR) and classification and regression tree (CART) were used to develop a pharmacogenomic algorithm for nateglinide dosing based on the published nateglinide pharmacokinetic data on the area under the curve data (AUC) and C_max (n = 143). CYP2C9 metabolizer phenotype, SLCO1B1, MTNR1B genotypes, and CYP2C9 inhibitor usage were used as the input variables. The results and associations were further confirmed by meta-analysis and in silico studies.</p><p><strong>Results: </strong>The MLR models of AUC and C_max explain 87.4% and 59% variability in nateglinide pharmacokinetics. The Bland and Altman analysis of the nateglinide dose predicted by these two MLR models showed a bias of ± 26.28 mg/meal. The CART algorithm was proposed based on these findings. This model is further justified by the meta-analysis showing increased AUCs in CYP2C9 intermediate metabolizers and SLCOB1 TC and CC genotypes compared to the wild genotypes. The increased AUC in SLCO1B1 mutants is due to decreased binding affinity of nateglinide to the mutant affecting the influx of nateglinide into hepatocytes. MTNR1B rs10830963 G-allele-mediated poor response to nateglinide is attributed to increased transcriptional factor binding causing decreased insulin secretion.</p><p><strong>Conclusion: </strong>CYP2C9, SLCO1B1, and MTNR1B genotyping help in optimizing nateglinide therapy based on this algorithm and ensuring safety and efficacy.</p>","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"1083-1091"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40674674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between thyroid hormones and central nervous system metabolism in physiological and pathological conditions.","authors":"Nadia Sawicka-Gutaj,&nbsp;Natalia Zawalna,&nbsp;Paweł Gut,&nbsp;Marek Ruchała","doi":"10.1007/s43440-022-00377-w","DOIUrl":"https://doi.org/10.1007/s43440-022-00377-w","url":null,"abstract":"<p><p>Thyroid hormones (THs) play an important role in the regulation of energy metabolism. They also take part in processes associated with the central nervous system (CNS), including survival and differentiation of neurons and energy expenditure. It has been reported that a correlation exists between the functioning of the thyroid gland and the symptoms of CNS such as cognitive impairment, depression, and dementia. Literature data also indicate the influence of THs on the pathogenesis of CNS diseases, such as Alzheimer's disease, epilepsy, depression, and Parkinson's disease. This review describes the relationship between THs and metabolism in the CNS, the effect of THs on the pathological conditions of the CNS, and novel options for treating these conditions with TH derivatives.</p>","PeriodicalId":166986,"journal":{"name":"Pharmacological reports : PR","volume":" ","pages":"847-858"},"PeriodicalIF":4.4,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40410936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}