共查询到20条相似文献，搜索用时 31 毫秒
1.
Michał Seweryn Karbownik Paweł Gunerka Paweł Turowski Maciej Wieczorek Edward Kowalczyk Wojciech Łężak Tadeusz Pietras 《Pharmacological reports : PR》2018,70(2):346-349
Background
Catalytic subunit delta of phosphoinositide 3-kinase, p110δ, encoded by the PIK3CD gene, was recently proposed as a target for pharmacological treatment of schizophrenia. Current antipsychotic drugs were found to decrease the mRNA expression of PIK3CD, but the mechanism of this process is not known. The aim of the study was to elucidate the mechanism by which antipsychotic drugs affect the mRNA expression of PIK3CD.Methods
The direct effect of haloperidol, clozapine, olanzapine, quetiapine and amisulpride on p110δ enzymatic activity was tested with a kinase assay, and the results were referenced against data on the mRNA expression of PIK3CD.Results
Haloperidol, clozapine, olanzapine and quetiapine, but not amisulpride, at the concentration of 20–80?μM, were found to significantly increase enzymatic activity of p110δ by up to two times in a dose-dependent manner. Linear regression analysis revealed that more than 40% of the variance in antipsychotic drugs-induced changes in the expression of PIK3CD mRNA was explained only by changes in antipsychotic drug-regulated p110δ enzymatic activity (p?=?0.011).Conclusions
Antipsychotic drugs differentially increase the enzymatic activity of p110δ. This effect is associated with that of mRNA expression of the PIK3CD gene. Drug-enzyme interaction may explain the effect of antipsychotic drugs on the expression of PIK3CD mRNA, however, further studies are needed to investigate this hypothesis. 相似文献2.
Takahiro Mizoguchi Hiroko Minakuchi Miyu Tanaka Kazuhiro Tsuruma Masamitsu Shimazawa Hideaki Hara 《Pharmacological reports : PR》2018,70(3):476-480
Background
VGF nerve growth factor inducible (VGF) is a neuropeptide which is expressed in neuronal cells and endocrine cells. VGF is induced by several neurotrophic factors. The expression level of VGF in patients with schizophrenia is increased in cerebrospinal fluid (CSF) and prefrontal cortex. In our previous study, we generated mice in which the expression level of VGF in the brain was increased. VGF-overexpressing mice exhibited abnormal behaviors including hyperactivity. However, it remains unknown whether VGF-overexpressing mice exhibit the endophenotype of schizophrenia and whether abnormal behaviors in these mice can be improved by antipsychotics.Methods
In the present study, we investigated schizophrenia-like behaviors and the responsiveness to antipsychotics in transgenic mice.Results
VGF-overexpressing mice (1) exhibited prepulse inhibition (PPI) impairment, (2) showed normalized hyperactivity following antipsychotic drug treatment, and (3) showed abnormal responsiveness to haloperidol.Conclusion
Upregulation of VGF may be implicated in the pathophysiology of schizophrenia and abnormalities of dopaminergic signaling. 相似文献3.
Background
Long term use of glucocorticoids is one of the most common causes of secondary osteoporosis. Osteocyte, the most abundant cell type in bone, coordinates the function of osteoblast and osteoclast. This study evaluates the protective effect of alpinumisoflavone (AIF), a naturally occurring flavonoid compound, on dexamethasone (Dex)-induced apoptosis of osteocytes.Methods
MLO-Y4 cell was used as a cell model. The effect of AIF on the cell viability was assessed by MTT assay. Apoptosis of MYL-Y4 cells was determined by DNA fragment detection ELISA kit and flow cytometry. Intracellular ROS level was determined by DCFH-DA staining. mRNA and protein expression of target genes were determined by qRT-PCR and western blot, respectively.Results
AIF effectively protected MLO-Y4 cells against Dex-induced apoptosis, which was associated with attenuation of Dex-induced ROS generation in MLO-Y4 cells. Furthermore, our data indicated that the expression of NAD(P)H oxidase 2 (Nox2) was suppressed by AIF, which in turn mediated the attenuating effect on Dex-induced ROS generation and apoptosis in MLO-Y4 cells. Moreover, our results showed that AIF modulated the expression of Nox2 by activating AMPK signaling.Conclusion
AIF activated AMPK-dependent Nox2 signaling pathway to suppress Dex-induced ROS production in cultured osteocytes, which might explain its anti-apoptotic effect. These results indicate that activation of AMPK pathway by AIF could have beneficial effects on bone damage induced by excessive oxidative stress and osteocyte apoptosis. 相似文献4.
Background
Limited data demonstrate the effect of nickel released from orthodontic appliances. The mechanism of this action is not clear. The present study aimed to investigate the role of kynurenines, oxidative stress and caspase pathway in the mechanism of nickel action.Methods
We studied the concentration of nickel, 3-hydroxykynurenine, total oxidative status in saliva and caspase-3 in epithelial cells in 10 subjects before and one week after orthodontic treatment.Results
Orthodontic appliances significantly enhanced the concentration of nickel, 3-hydroxykynurenine, total oxidative status and augmented the expression of caspase-3 seven days after treatment in the oral cavity in respect to pre-treatment values.Conclusion
Our data suggest that nickel released from orthodontic appliances activate tryptophan metabolism in oral cavity via the kynurenine pathway. The metal directly or through kynurenines enhancement activates oxidative stress and then via the caspase pathway induce apoptosis of buccal epithelial cells. 相似文献5.
Elżbieta Gałecka Monika Talarowska Michael Maes Kuan-Pin Su Paweł Górski Anna Kumor-Kisielewska Janusz Szemraj 《Pharmacological reports : PR》2018,70(1):133-138
Background
Thyroid hormones (TH) are involved in modulation of the immune system and inflammation. TH dysregulation is associated with depressive disorders. The iodothyronine deiodinases (DIOs), the key enzymes for TH synthesis, can be affected and induced by pro-inflammatory cytokines. We aimed to investigate the levels of and correlation between type 2 DIO (DIO2) and interferon-gamma (IFN-?) in patients with recurrent depressive disorders (rDD).Methods
Data from 91 rDD patients and 105 healthy controls were analyzed. The diagnoses are based on the ICD-10 criteria (F33.0-F33.8). Expression levels of DIO2 and IFN-? were estimated using the method based on the polymerase chain reaction and the enzyme-linked immunosorbent assay (ELISA).Results
The DIO2 expression on mRNA/protein levels in rDD patients (both female and males) was reduced as compared with the control subjects. No correlation between DIO2 and IFN-? expression was observed.Conclusion
This is the first study to reveal that one may cautiously suggest that DIO2 may be involved in the development and/or progression of rDD. The mechanisms of TH regulation on depression, however, need further investigation. 相似文献6.
Xiang-Fan Chen Xiao-Li Li Jin-Xin Liu Jing Xu Yan-Yan Zhao Min Yang Yan Zhang 《Pharmacological reports : PR》2018,70(4):705-711
Background
This study aimed to study the osteo-preservative effects of captopril, an inhibitor on angiotensin-converting enzyme (ACE), on bone mass, micro-architecture and histomorphology as well as the modulation of captopril on skeletal renin-angiotensin system (RAS) and regulators for bone metabolism in mice with bilateral orchidectomy.Methods
The orchidectomized (ORX) mice were orally administered with vehicle or captopril at low dose (10 mg/kg) and high dose (50 mg/kg) for six weeks. The distal femoral end, the proximal tibial head and the lumbar vertebra (LV) were stained by hematoxylin and eosin, Safranin O/Fast Green and masson-trichrome. Micro-computed tomography was performed to measure bone mineral density (BMD).Results
Treatment with captopril increased trabecular bone area at distal metaphysis of femur, proximal metaphysis of tibia and LV-4, moreover, high dose of captopril significantly elevated trabecular BMD of LV-2 and LV-5. The mRNA expressions of renin receptor, angiotensinogen, carbonic anhydrase II, matrix metalloproteinase-9, and tumor necrosis factor-alpha were significantly decreased in tibia of ORX mice following treatment with captopril. The administration with captopril enhanced the ratio of OPG/RANKL mRNA expression, the mRNA expression of transforming growth factor-beta and the protein expression of bradykinin receptor-1.Conclusions
The inhibition on ACE by captopril exerts beneficial effects on trabecular bone of ORX mice. The therapeutic efficacy may be attributed to the regulation of captopril on local RAS and cytokines in bone. 相似文献7.
Isabella dos Santos Guimarães Taciane Ladislau-Magescky Nayara Gusmão Tessarollo Diandra Zipinotti dos Santos Etel Rodrigues Pereira Gimba Cinthya Sternberg Ian Victor Silva Leticia Batista Azevedo Rangel 《Pharmacological reports : PR》2018,70(3):409-417
Background
Epithelial ovarian cancer (EOC) remains the most lethal gynecologic malignancy. Primary cytoreductive surgery with adjuvant taxane-platinum chemotherapy is the standard treatment to fight ovarian cancer, however, their side effects are severe, and chemoresistance emerges at high rates. Therefore, EOC clinic urges for novel treatment strategies to reverse chemoresistance and to improve the survival rates. Metformin has been shown to act in synergy with certain anti-cancer agents, overcoming chemoresistance in various types of tumors. This paper aims to investigate the use of metformin as a new treatment option for cisplatin- and paclitaxel-resistant ovarian cancer.Methods
The effects of metformin alone or in combination with conventional drugs on resistant EOC cell lines were investigated using the MTT assay for cell proliferation; Flow Cytometry analysis for cell cycle and the mRNA expression was analyzed using the real-time PCR technique.Results
We found that metformin exhibited antiproliferative effects in paclitaxel-resistant A2780-PR, and in cisplatin-resistant ACRP cell lines. The combined therapy containing conventional drugs and metformin improved the effect of the treatment in cell proliferation rate, especially in the resistant cells. We found that metformin, in clinical relevant doses, could significantly reduce the mRNA expression of inflammatory cytokines and NF-κB signaling pathway.Conclusions
Taken together, our observations suggest that metformin inhibits the inflammatory pathway induced by paclitaxel and cisplatin treatment. Furthermore, metformin in combination with paclitaxel or cisplatin improved the sensitivity in drug-resistant ovarian cancer cells. Therefore, metformin may be beneficial treatment strategy, particularly in patients with tumors refractory to platinum and taxanes. 相似文献8.
Inci Kazkayasi Nihan Burul-Bozkurt Muhammad-Al-Mustafa Ismail Paula Merino-Serrais Can Pekiner Angel Cedazo-Minguez Serdar Uma 《Pharmacological reports : PR》2018,70(4):677-683
Background
Many studies have indicated a relationship between diabetes and Alzheimer’s disease (AD). However, the molecular mechanism underlying this association has not been clarified. Among several factors, insulin degrading enzyme (IDE), which plays roles in the degradation of both insulin and amyloid β (Aβ), has gained interest as a potential target in efforts to solve this puzzle. This study sought to examine the effects of varying insulin and/or glucose concentrations on IDE expression.Methods
Experiments were performed on primary cultured rat neurons and cortices of rats with streptozotocin (STZ)-induced diabetes. IDE protein and mRNA expression levels were measured by western blot and RT-PCR, respectively.Results
In primary cultured cortical neurons, removal of insulin for 5 days reduced the expression of IDE. A five-day treatment with a high concentration of glucose in insulin-free media reduced IDE levels, while a high concentration of glucose in the presence of insulin had no effect. In groups treated with glucose or insulin intermittently, the reduction in IDE levels was observed only in neurons exposed to high glucose together with no insulin for 5 days. Shorter incubation periods (48 h), either continuously or intermittently, did not affect IDE levels. IDE expression in the cortex of rats with STZ-induced diabetes was found to be decreased.Conclusion
Our data suggest that insulin deprivation, rather than high glucose, is a significant determinant of IDE regulation. As evidence indicates potential roles for IDE in diabetes and AD, understanding the mechanisms regulating IDE expression may be important in developing new treatment strategies. 相似文献9.
Angelika Długosz Katarzyna Gach-Janczak Jacek Szymański Dariusz Deredas Tomasz Janecki Anna Janecka 《Pharmacological reports : PR》2018,70(4):631-638
Background
The development of multidrug resistance to chemotherapy remains a challenge in the treatment of cancer and is a major factor causing failure of many forms of chemotherapy. The ATP binding cassette (ABC) family of proteins are efflux pumps that transport various potentially dangerous substances out of the cells. Several of the ABC transporters are related to chemoresistance, as the rapidly dividing malignant cells use them to protect themselves from medical interventions. Inhibitors of ABC transporters have the potential to enhance the efficacy of anticancer drugs. Two new synthetic compounds, AD-06 and AD-013, were tested as possible multidrug resistance inhibitors in MCF-7 cells.Methods
The cytotoxicity of new compounds was tested in MCF-7 and MCF-10A cell lines using the MTT method. Gene expression was measured by real-time PCR and changes in the protein levels were evaluated by flow cytometry and ELISA. A method based on the use of a fluorescent dye, being a marker of the ABC transporter activity, was used for screening the tested compounds as potential multidrug resistance inhibitors.Results
AD-06 and AD-013 down-regulated NF-κB mRNA levels and decreased the population of cells with activated NF-κB. Both compounds were found to be strong ABCB1 and ABCG2 transporter inhibitors. They showed synergistic effects when incubated with taxol or oxaliplatin.Conclusions
α-Methylene-γ- and -δ-lactones AD-06 and AD-013 are promising lead structures for further development as multidrug resistance inhibitors. 相似文献10.
Ryszard Pluta Anna Bogucka-Kocka Marzena Ułamek-Kozioł Jacek Bogucki Sławomir Januszewski Janusz Kocki Stanisław J. Czuczwar 《Pharmacological reports : PR》2018,70(5):881-884
Background
Tauopathies are a class of neurodegenerative illnesses associated with the aberrant accumulation of the tau protein in the brain. The best known out of these diseases is Alzheimer’s disease, a disorder where the microtubule associated tau protein becomes hyperphosphorylated (which lowers its binding affinity to microtubules) and accumulates inside neurons in the form of tangles. In this study, we attempt to find out whether brain ischemia may play an important role in tau protein gene alterations.Methods
We have investigated the relationship between hippocampal ischemia and Alzheimer’s disease by means of a transient 10-min global brain ischemia in rats and determining the effect on Alzheimer’s disease tau protein gene expression during 2, 7 and 30?days post injury.Results
We found the significant overexpression of tau protein gene on the 2nd day, but on day’s 7 and 30 post-ischemia there a significant opposite tendency was observed.Conclusion
The obtained results offer a novel insight into tau protein gene in regulating delayed neuronal death in the ischemic hippocampus. Finally, these findings further elucidate the long-term impact of brain ischemia on Alzheimer’s disease development. 相似文献11.
Anna Leja-Szpak Katarzyna Nawrot-Porąbka Marta Góralska Martyna Jastrzębska Paweł Link-Lenczowski Joanna Bonior Piotr Pierzchalski Jolanta Jaworek 《Pharmacological reports : PR》2018,70(6):1079-1088
Background
Gemcitabine is a standard chemotherapeutic agent for patients suffering from pancreatic cancer. However, the applied therapy is not effective due to the resistance of tumor cells to cytostatics, caused by inefficiency of the apoptotic mechanisms. Herein, we present the hypothesis that melatonin and its metabolite N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) modify the effect of gemcitabine on PANC-1 cells and that this phenomenon is dependent on the modulation of apoptosis.Methods
PANC-1 cells have been incubated with melatonin, AFMK or gemcitabine alone or in combination to determine the cytotoxity and proliferative effects. In subsequent part of the study, cells were harvested, the proteins were isolated and analyzed employing immunoprecipitation/immunoblotting.Results
Incubation of PANC-1 cells with gemcitabine resulted in upregulation of pro-apoptotic bax and caspases proteins expression, downregulation of anti-apoptotic Bcl-2, heat shock proteins (HSPs) and modulation of cellular inhibitors of apoptosis (IAPs). Both melatonin and AFMK administered to PANC-1 in combination with gemcitabine inhibited the production of HSP70 and cIAP-2 as compared to the results obtained with gemcitabine alone. These changes were accompanied by upregulation of Bax/Bcl-2 ratio and reduction of procaspases-9 and -3 abundance, followed by an increase in the formation of active caspase of PANC-1 cells with combination of gemcitabine plus low doses of melatonin or AFMK led to enhanced cytotoxicity and resulted in the inhibition of PANC-1 cells growth as compared to effects of gemcitabine alone.Conclusion
Melatonin and AFMK could improve the anti-tumor effect of gemcitabine in PANC-1 cells presumably through the modulation of apoptotic pathway. 相似文献12.
13.
Tomasz Kocki Ewa M. Urbańska Janusz Kocki Renata Kloc Katarzyna Kocka Marcin Olajossy Björn Owe-Larsson 《Pharmacological reports : PR》2018,70(4):737-745
Background
Accumulating data suggest an important role of disturbed kynurenine pathway and altered glutamatergic transmission in the pathogenesis of depression. In here, we focused on detailed analyses of kynurenic acid (KYNA) status in vivo following single and 14-day administration of selected tricyclic antidepressant drugs (TCAs) and serotonin selective reuptake inhibitors (SSRIs) in rats.Methods
The effect of antidepressants on serum and brain KYNA levels, as well as on the activity of kynurenine aminotransferases (KATs I and II) and expression of Kat1 and Kat2 genes mRNA was studied in three brain regions.Results
Chronic, but not acute, application of antidepressants invariably stimulated KYNA production in hippocampus (amitriptyline, imipramine, fluoxetine and citalopram) and sporadically in cortex (amitriptyline, fluoxetine), whereas no change in KYNA level was observed in striatum. Cortical and hippocampal expression of Kat1 and Kat2 genes was increased after chronic, but not single administration of all studied antidepressants. The activity of semi-purified enzymatic proteins, KAT I and II, was not paralleling changes of Kat1 and Kat2 genes.Conclusion
Our data indicate that prolonged administration of antidepressants targets expression of KYNA biosynthetic enzymes. Furthermore, post-translational modulation of KATs seems to play an important role in tuning of KYNA synthesis within brain structures. We suggest that consistent increase of hippocampal KYNA levels may represent hallmark of antidepressant activity. Mechanisms governing region- and drug-selective action of antidepressants require further investigations. 相似文献14.
Meizhi Wang Hui Gao Haijun Qu Jing Li Kaili Liu Zhiwu Han 《Pharmacological reports : PR》2018,70(5):963-971
Background
The most frequent type of renal cell carcinoma is called clear-cell renal cell carcinoma (ccRCC) which is associated with a poor prognosis. It has been observed that miR-137 is aberrantly expressed in many different kinds of human malignancies including ccRCC. This research aims to examine the role of miR-137 in ccRCC.Methods
Quantitative RT-PCR (qRT-PCR) was applied to measure miR-137 expression in ccRCC and adjacent noncancerous tissue. Gene expression was determined by western blot. Cell Counting Kit-8 (CCK-8) assay, flow cytometry and Transwell assay were used to determine the effects of miR-137 on cell growth, apoptosis and invasion, respectively. Moreover, xenograft and pulmonary metastasis animal models were established to investigate the role of miR-137 in vivo.Results
Our findings show that there was significant downregulation of miR-137 in ccRCC tissue relative to corresponding non-cancerous tissue. Ectopic miR-137 expression in ccRCC cells led to suppression of cell growth and invasion, as well as apoptosis induction. In contrast, knockdown of miR-137 enhances proliferation and invasion, inhibits apoptosis. It also confirms that miR-137 plays a tumor supressor role in vivo. Mechanically, miR-137 directly targets the 3′-UTR of RLIP76 which is an established oncogene in ccRCC.Conclusion
MiR-137 serves as a tumor suppressor, which can be considered a potential therapeutic target in ccRCC. 相似文献15.
Enrique Gallego-Colon Agnieszka Klych-Ratuszny Agnieszka Kosowska Wojciech Garczorz Mohammad Reza F. Aghdam Michal Wozniak Tomasz Francuz 《Pharmacological reports : PR》2018,70(1):178-183
Background
Incretin analogue drugs, a FDA-approved treatment in diabetes, has been tested for its therapeutic properties as modulators of atherosclerosis. We investigated the effects of incretin drugs on the modulation of gene expression and protein levels of matrix metalloproteinases (MMPs) as well as their inhibitors ? tissue inhibitors of metalloproteinases (TIMPs) in coronary artery smooth muscle cells (hCASMC) in the context of atherosclerotic plaque formation and inflammation.Methods
TNFα-stimulated hCASMC were treated with Glucagon-like Peptide 1 (GLP-1) (10 nM and 100 nM) and Exendin-4 (1 nM and 10 nM). Messenger RNA (mRNA) levels and protein concentrations of MMP-1, MMP-2, MMP-9 and TIMP-1, TIMP-2 were measured and the effects on extracellular matrix turnover under TNFα-mediated microenvironment were evaluated. Intracellular signaling pathways were also examined.Results
Our experiments reveal that GLP-1 receptor agonists downregulate the expression of MMP-1, MMP-2, MMP-9 in hCASMC under TNFα mediated inflammatory conditions. Signaling pathway analysis show that GLP-1 receptor agonists induced inhibition of AKT-Thr308 phosphorylation, PRAS40 and S6 proteins but not AKT-Ser473.Conclusions
These findings indicate that GLP-1 receptor agonists modulate the expression of MMPs through inhibition of AKT-Thr308 phosphorylation in hCASMC. These results suggest a possible role of incretin analogue drugs in therapy of coronary atherosclerosis. 相似文献16.
Amir Afkham Leili Aghebati-Maleki Homayoon Siahmansouri Sanam Sadreddini Majid Ahmadi Sanam Dolati Nahid Manafi Afkham Parvin Akbarzadeh Farhad Jadidi-Niaragh Vahid Younesi Mehdi Yousefi 《Pharmacological reports : PR》2018,70(3):418-425
Background
Prostate cancer is known as the most common malignancy in men. Chitosan has generated great interest as a useful biopolymer for the encapsulation of small interfering RNA (siRNA). Due to cationic nature, chitosan is able to efficiently encapsulate siRNA molecules and form nanoparticles. Furthermore, the biocompatible and biodegradable attributes of chitosan have paved the way for its potential application in the in vivo delivery of therapeutic siRNAs. In this study, we aimed to design chitosan/CMD nanoparticles for the efficient encapsulation of the anti-cancer drugs SN38 and Snail-specific siRNA.Methods
Physicochemical characteristics, growth inhibitory properties, and anti-migratory capacities of the dual delivery of SN38-Snail siRNA CMD-chitosan nanoparticles were investigated in prostate cancer cells.Results
Our findings provided evidence for the suggestion that, ChNP-CMD-SN38-siRNA treated cells, the mRNA level of snail decreased from 1.00 to 0.30 (±0.14) and 0.09 (±0.04) after 24 h and 48 h, respectively. Additionally, the fold induction of E-cadherin and Claudin-1 increased from 1.00 to now 3.12 (±0.62), 3.02 (±0.28) after 24 h and 5.6 (±0.91), 4.42 (±0.51) after 48 h, respectively. Also, co-delivery of SN38 and Snail-specific siRNA by an appropriate nanocerrier (chitosan nanoparticles) could reduce the viability, proliferation, and migration of PC-3 cells.Conclusions
In conclusion, ChNPs encapsulating SN38 and Snail-specific siRNA may represent huge potential as an effective anti-cancer drug delivery system for the treatment of prostate cancer. 相似文献17.
Xiao-Jie Bai Jun-Tao Hao Jin Wang Wei-Fang Zhang Cai-Ping Yan Jia-Hui Zhao Zhi-Qing Zhao 《Pharmacological reports : PR》2018,70(1):60-68
Background
This study tested the hypothesis that inhibition of cardiac hypertrophy and preservation of cardiac/endothelial function by the natural yellow pigment curcumin are associated with upregulated expression of Na+/Ca2+ exchanger (NCX) after transverse aortic constriction (TAC).Methods
Male Wistar rats were subjected to TAC for 10 weeks and curcumin (50?mg/kg/day) was fed by gastric gavage during TAC. Expression of NCX and endothelial nitric oxide synthase (eNOS) was analyzed by Western blot and immunohistochemistry.Results
Compared with the animals in the TAC group, curcumin significantly increased the survival rate and reduced the ratio of heart or left ventricle (LV) to body weight and the cross sectional area of cardiomyocytes. In coincidence with improved LV systolic pressure and reduced LV end-diastolic pressure, curcumin significantly reduced LV end-systolic and diastolic diameter/dimension, and enhanced LV ejection fraction and LV fractional shortening as measured by echocardiography. Furthermore, endothelium-dependent relaxation of aortic rings in response to acetylcholine was significantly improved by curcumin. Along with these modifications, the expression and localization of NCX and eNOS in the myocardium and vascular endothelium were significantly upregulated by curcumin. The protective effect of curcumin on endothelium-dependent relaxation was partly blocked by pretreatment with the NCX inhibitor, KB-R7943.Conclusions
These results demonstrate that inhibition of cardiac hypertrophy, improvement of cardiac systolic/diastolic function and preservation of vascular endothelium by curcumin might be associated with upregulated NCX expression level in response to increased afterload. 相似文献18.
Karolina Noworyta-Sokołowska Anna Maria Górska Krystyna Gołembiowska 《Pharmacological reports : PR》2018,70(5):890-895
Background
According to the European Drug Report, the use of novel psychoactive substances (NPS) is constantly growing. NPS are widely abused by human adolescent subjects. 5-Methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT) is one of the most frequently used hallucinogenic NPS. 5-MeO-DIPT intoxication results in hallucinations, vomiting, and tachycardia. Long-term exposure to 5-MeO-DIPT was reported to lead to development of post-hallucinogenic perception disorder.The aim of the present study was to determine whether repeated-intermittent administration of 5-MeO-DIPT during adolescence affects learning and memory in adult rats.Methods
Rats were treated with 5-MeO-DIPT in a dose of 2.5 mg/kg from 30 to 33 and 37 to 40 Postnatal Day (PND). The experiments were conducted when the animals reached 90 PND. The effect of 5-MeO-DIPT on cognitive functions was assessed using the novel object recognition, open field, and serial pattern learning (SPL) tests.Results
Repeated-intermittent exposure to 5-MeO-DIPT during adolescence decreased the number of crossings in the open field test at adulthood. Moreover, 5-MeO-DIPT treatment impaired adult rats’ learning in the SPL test. There was no change in the novel object recognition test.Conclusions
The present results show that the performance of adult rats treated with 5-MeO-DIPT during adolescence was impaired in the open field test, which indicates the attenuated exploratory activity. 5-MeO-DIPT treatment undermined adult rats’ performance in the serial pattern learning test, suggesting impairment of long term memory and cognitive flexibility. The present study showed that the exposure to 5-MeO-DIPT during adolescence might lead to long-lasting behavioral changes which persisted long after the exposure period. 相似文献19.
Jin-nan Zhong Lan Lan Yi-fei Chen Ge Huang Guang-zhen He Jiong Yang Ya-dong Gao 《Pharmacological reports : PR》2018,70(1):22-28
Background
Circulating fibrocytes (CFs) have been shown to participate in subepithelial fibrosis of asthma with chronic airflow limitation by acting as an important source of fibroblasts deposited beneath airway epithelia. Serum amyloid P (SAP) is an innate inhibitor of fibrocytes differentiation. Store-operated Ca2+ entry (SOCE) is the major Ca2+ influx of non-excitable cells. In this study, the role of SOCE in the regulation of fibrocytes differentiation and the effects of Th2 cytokine IL-4 and SAP on SOCE of fibrocytes were investigated.Methods
Peripheral blood mononuclear cells or monocytes were cultured in serum-free medium for 7 days to differentiate into fibrocytes; the expression of SOC channels was determined with PCR, SOCE was measured with Ca2+ fluorescence imaging.Results
IL-4 significantly promoted monocyte derived fibrocytes differentiation in vitro. It also increased both SOCE which was induced by thapsigargin or UTP and molecules STIM1 and Orai1 which were related to expression of SOC channels in fibrocytes. Fibrocytes differentiation induced by IL-4 and SOC channels activity could be inhibited by SOC channel blocker SKF-96365. As expected, SAP significantly inhibited IL-4-induced differentiation of fibrocytes, the activity of SOCE and the expression of STIM1 and Orai1 in IL-4-treated fibrocytes.Conclusion
IL-4 and SAP reversely regulates cultured fibrocytes differentiation in vitro by respectively promoting or inhibiting the expression and activity of SOC channels in fibrocytes. 相似文献20.
Zekrayat J.H. Medras Norhan M. El-Sayed Sawsan A. Zaitone Eman A. Toraih Manal M. Sami Yasser M. Moustafa 《Pharmacological reports : PR》2018,70(2):233-242