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1.
Ártur Krumberg Schüller Diego Antonio Mena Canata Fernanda Schäfer Hackenhaar Vanessa Krüger Engers Fernanda Maciel Heemann Jordana Salete Putti Tiago Boeira Salomon Mara Silveira Benfato 《Pharmacological reports : PR》2018,70(2):263-269
Background
Bilateral ovariectomy is an experimental model used to analyse the effects of menopause and develop strategies to mitigate the deleterious effects of this condition. Supplementation of the diet with antioxidants has been used to reduce potential oxidative stress caused by menopause. The purpose of the study was to analyse the effects of α-lipoic acid (LA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), dietary supplementation on oxidative stress in the livers of ovariectomized rats.Methods
In this study, we evaluated the effect of dietary supplementation with LA, DHA and EPA for a period of 16 weeks on oestrogen levels and oxidative stress biomarkers in the livers of ovariectomized 25 three-month-old rats.Results
Serum oestrogen levels were lower after ovariectomy but were not altered by dietary treatments. LA was capable of acting in the liver, recovering the activity of the antioxidant enzymes superoxide dismutase and glutathione peroxidase, and reducing protein oxidative damage. Moreover, LA supplementation reduced nitrite and nitrate levels. DHA and EPA recovered the antioxidant activity of cytosolic and mitochondrial superoxide dismutase, decreasing protein oxidation. Protection against lipid oxidation differed between treatments. The DHA-treated group showed increased levels of the lipid peroxidation biomarker malondialdehyde compared to the ovariectomized group. However, malondialdehyde levels were not altered by EPA treatment.Conclusions
The results suggest that the antioxidant response varies among evaluated supplementations and all supplements were able to alter enzymatic and non-enzymatic antioxidants in the livers of ovariectomized rats. DHA presented the most evident antioxidant effect, decreasing protein and lipid damage. 相似文献2.
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3.
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4.
Background
Well known risk factors for diabetic erectile dysfunction include impaired nitric oxide synthesis and endothelial dysfunction. We proposed to evaluate the efficacy of nitric oxide donor, molsidomine in rat model of diabetic erectile dysfunction.Methods
Streptozotocin (52 mg/kg, ip) induced diabetic male rats were treated with molsidomine (5 and 10 mg/kg, po) for 8 weeks. The sexual behaviour of male rat in presence of the female rat in oestrous phase was observed at the end of study. The effect of treatment on serum testosterone level, sperm parameters and penile tissue histopathology was also evaluated. Further anti-inflammatory activity and antioxidant potential of molsidomine was evaluated by in vitro method. In silico docking study was carried out to appreciate binding conformation of the molsidomine to its plausible target, phosphodiesterase enzyme.Results
Molsidomine significantly and dose dependently increased sexual behaviour, sperm count and serum testosterone level in diabetic rats. Further, the protective effect of molsidomine was also substantiated by pathological changes in the architect of the penile tissue. Molsidomine showed good membrane stability accounting for its significant anti-inflammatory action and also significantly scavenged DPPH radical activity showing its antioxidant action. Molsidomine was found to settle well in the active site of PDE-5 enzyme with less binding affinity than the standard drug sildenafil.Conclusion
The results highlight the rationale behind the repositioning of molsidomine therapy for the management of diabetic erectile dysfunction. 相似文献5.
Magnesium sulfate reduces formalin-induced orofacial pain in rats with normal magnesium serum levels
Dragana P. Srebro Sonja M. Vučković Ivan S. Dožić Branko S. Dožić Katarina R. Savić Vujović Aleksandar P. Milovanović Branislav V. Karadžić Milica Š. Prostran 《Pharmacological reports : PR》2018,70(1):81-86
Background
In humans, orofacial pain has a high prevalence and is often difficult to treat. Magnesium is an essential element in biological a system which controls the activity of many ion channels, neurotransmitters and enzymes. Magnesium produces an antinociceptive effect in neuropathic pain, while in inflammatory pain results are not consistent. We examined the effects of magnesium sulfate using the rat orofacial formalin test, a model of trigeminal pain.Methods
Male Wistar rats were injected with 1.5% formalin into the perinasal area, and the total time spent in pain-related behavior (face rubbing) was quantified. We also spectrophotometrically determined the concentration of magnesium and creatine kinase activity in blood serum.Results
Magnesium sulfate administered subcutaneously (0.005–45 mg/kg) produced significant antinociception in the second phase of the orofacial formalin test in rats at physiological serum concentration of magnesium. The effect was not dose-dependent. The maximum antinociceptive effect of magnesium sulfate was about 50% and was achieved at doses of 15 and 45 mg/kg. Magnesium did not affect increase the levels of serum creatine kinase activity.Conclusions
Preemptive systemic administration of magnesium sulfate as the only drug can be used to prevent inflammatory pain in the orofacial region. Its analgesic effect is not associated with magnesium deficiency. 相似文献6.
Abdulkadir Tasdemir Mehmet Taskiran Nusret Ayyildiz 《Pharmacological reports : PR》2018,70(5):885-889
Background
The most common headache associated with epilepsy occurs after seizure activity and is called a postictal headache. Therefore, the objective of this study was to investigate the effects of low and high doses acetylsalicylic acid (aspirin) on a penicillin-induced experimental epilepsy model.Methods
Adult male Wistar rats (n?=?28, weighing 220?±?40?g) were used in the experiments. The rats were divided into four groups as Control, Penicillin, Aspirin 150?mg/kg, Aspirin 500?mg/kg. Seizure activity was triggered by an intracortical injection of penicillin G potassium (500?IU/2.5?μl) into the sensory motor cortex. An electrocorticogram was recorded by using conductive screw electrodes. Aspirin at the doses of 500?mg/kg and 150?mg/kg was given intraperitoneally (ip) 30?min after penicillin administration.Results
Anticonvulsant activity appeared at the 30th and 40th min after an intracortically administered injection of penicillin in the groups given aspirin doses of 500?mg/kg (ip) and 150?mg/kg (ip) respectively. The amplitude of epileptiform activity at both doses of aspirin decreased but the difference was not statistically significant.Conclusions
The results of the present study suggest that low and high doses of aspirin may decrease epileptiform activity in penicillin-induced epilepsy. Aspirin might be suggested for headache associated with epilepsy. 相似文献7.
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8.
Sumin Yang Changhun Lee Bong-Seon Lee Eui Kyun Park Kyung-Min Kim Jong-Sup Bae 《Pharmacological reports : PR》2018,70(6):1195-1201
Background
Aspalathin (Aspt) and nothofagin (Not) were reported to have antioxidant activity and are the two major active dihydrochalcones in green rooibos. This study was conducted to determine whether Asp and Not can modulate renal functional damage in a mouse model of sepsis and to elucidate the underlying mechanisms.Methods
The potential of Aspt and Not treatment to reduce renal damage induced by cecal ligation and puncture (CLP) surgery in mice was measured by assessing blood urea nitrogen (BUN), serum creatinine, total urine protein, levels of lactate dehydrogenase (LDH), nitric oxide (NO), tumour necrosis factor (TNF)-α, interleukin (IL)-6, and myeloperoxidase (MPO), lipid peroxidation, total glutathione, glutathione peroxidase activity, catalase activity, and superoxide dismutase activity.Results
Treatment with Aspt and Not decreased plasma levels of BUN, creatinine, urine protein, and LDH in mice with CLP-induced renal damage. Moreover, Aspt and Not inhibited nuclear factor (NF)-κB activation and reduced the induction of NO synthase and excessive production of nitric acid. Aspt and Not treatment also reduced the plasma levels of NO, TNF-α,?IL-6, and MPO and reduced lethality due to CLP-induced sepsis, increased lipid peroxidation, and markedly enhanced the antioxidant defence system by restoring the levels of superoxide dismutase, glutathione peroxidase, and catalase in the kidney tissues.Conclusion
Our results suggest that Aspt and Not protect mice against sepsis-triggered renal injury. 相似文献9.
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10.
Jinyan Han Ping Zhao Weiqin Shao Zengmin Wang Fengxue Wang Lei Sheng 《Pharmacological reports : PR》2018,70(5):853-862
Background
Acute lymphoblastic leukemia (ALL) is the most common fatal cancer in people younger than 20 years of age. This study was designed to explore the anti-leukemia activity of physcion 8-O-β-glucopyranoside (PG) in B-cell ALL.Methods
NALM6 and SupB15 cells were used as model cell lines. Cell viability, cell apoptosis, cell cycle distribution were determined by CCK-8 assay, DNA fragmentation assay and flow cytometry, and flow cytometry, respectively. Expression of proteins involved in cell apoptosis and cell cycle regulation was determined by western blot and the levels of ceramide and sphingosine 1-phosphate (S1P) were determined by ELISA. Activity of sphingosine kinase 1 (SphK1) was also determined with a Sphingosine Kinase Assay Kit. In the present study, both model cell lines were transfected with siRNA targeting SphK1 or an overexpression plasmid to examine the role of SphK1 in the anti-leukemia activity of PG. Moreover, the efficacy of PG was examined in vivo in a mouse model by measuring survival and spleen weight.Results
Our results provided experimental evidence that PG could significantly induce apoptosis and cell cycle arrest in vitro. Mechanistically, the anti-leukemia activity of PG was mediated by its ability to repress SphK1 and thus modulate ceramide-S1P rheostat. Moreover, the anti-leukemia activity of PG was also verified in a murine model.Conclusion
Collectively, our results indicate that PG may be a promising agent for the treatment of B-cell leukemia. 相似文献11.
Background
Elevated prolactin levels are associated with sexual dysfunction in women. No previous study has investigated the effect of dopamine agonists on sexual functioning in women.Methods
The study enrolled 30 young women with mild hyperprolactinemia (serum prolactin levels in the range between 25 and 50 ng/mL), 15 of whom were later treated with bromocriptine (5–10 mg daily), as well as 14 age- and weight-matched healthy women. All women completed a questionnaire evaluating female sexual function (Female Sexual Function Index – FSFI) and a questionnaire evaluating the presence and severity of depressive symptoms (Beck Depression Inventory Second Edition – BDI-II).Results
Women with mild hyperprolactinemia had a lower total FSFI score, lower scores in all domains of sexual functioning (desire, arousal, lubrication, and dyspareunia), as well as a lower total BDI-II score than control women. Bromocriptine increased the FSFI score and tended to reduce BDI-II score. Moreover, the drug normalized desire, arousal, lubrication and dyspareunia, as well as improved orgasm and sexual satisfaction and this action correlated with changes in prolactin levels and an improvement in insulin sensitivity. No changes in sexual functioning and depressive symptoms were observed in untreated women with mild hyperprolactinemia and healthy controls.Conclusions
Bromocriptine treatment improves female sexual functioning and slightly affects depressive symptoms in women with elevated prolactin levels and this effect is related to its prolactin-lowering and metabolic effects. 相似文献12.
Naeima Eftekhar Ali Moghimi Mohammad Hossein Boskabady 《Pharmacological reports : PR》2018,70(1):119-125
Background
Rosmarinic acid (RA) as an active component of several medicinal plants, has shown anti-inflammatory and anti-oxidant effects. In this study, the effect of RA on tracheal responsiveness (TR), lung inflammatory cells, oxidant biomarkers in sensitized rats were evaluated.Methods
TR to methacholine and ovalbumin (OVA) as well as total and differential white blood cell (WBC) count and levels of nitrogen dioxide, nitrate, malondialdehyde, thiol, superoxide dismutase, and catalase in bronchoalveolar lavage fluid were measured in control (group?C) rats, sensitized animals to OVA and given drinking water alone (group S), S groups receiving drinking water containing three concentrations of RA (0.125, 0.250 and 0.500?mg/mL) and dexamethasone (1.25?μg/mL), (n?=?6 in each group).Results
Increased TR to methacholine and OVA, total WBC count, percentages of eosinophils, monocytes, neutrophils and levels of oxidant biomarkers but decreased other measured parameters were observed in group S compared to group C. Percentages of lymphocytes and antioxidant biomarkers were significantly increased but other measured parameters were significantly decreased in S group treated with dexamethasone and in rats treated with the two higher concentrations of RA compared to S group. The effect of RA medium concentration on percentage of eosinophils and RA high concentration on total WBC count and percentages of eosinophils and lymphocytes, were significantly higher than those of dexamethasone.Conclusion
These results showed the concentration-dependent effect of RA on tracheal responses, lung inflammatory cells and oxidant-antioxidant parameters which was comparable to that of dexamethasone at used concentrations in sensitized rats. 相似文献13.
Marta Jóźwiak-Bębenista Magdalena Jasińska-Stroschein Edward Kowalczyk 《Pharmacological reports : PR》2018,70(5):1032-1039
Background
Recent evidence suggests that the mitogen activated protein kinase (MAPK)-associated signaling pathway in the frontal cortical areas demonstrates abnormal activity in cases of schizophrenia. Moreover, schizophrenia patients often display alterations in the regional cellular energy metabolism and blood flow of the brain; these are shown to parallel changes in angiogenesis primarily mediated by vascular endothelial growth factor (VEGF).Methods
The present study examines the differential effects of time-dependent treatment with haloperidol, olanzapine and amisulpride (20 μM) on VEGF and MAPK mRNA expression and VEGF level, using the T98 cell line as an example of nerve cells. For the purposes of comparison, the effect of neuroprotective pituitary adenylate cyclase-activating polypeptide (PACAP) on the expression of VEGF mRNA and secretion were also evaluated in this cell model.Results
RT-PCR analysis revealed that all the tested neuroleptics increased VEGF mRNA expression after 72-h incubation; however, only haloperidol and olanzapine also increased the level of VEGF detected by ELISA, and they demonstrated significantly stronger effects than PACAP. Haloperidol and olanzapine, but not amisulpride, decreased MAPK14 mRNA expression in T98G cells after 72-h incubation.Conclusion
The obtained results suggest that haloperidol and olanzapine can trigger the MAPK and VEGF signaling pathway, which may contribute to their neuroprotective mechanism of action. 相似文献14.
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15.
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16.
Background
Methylene-tetrahydrofolate reductase (MTHFR) gene variant may play an important role in the pathophysiology of diabetes and its complications due to its influence on plasma homocysteine levels and also its effect on scavenging peroxynitrite radicals. Diabetic peripheral neuropathy (DPN) is one of the most common diabetic chronic complications. The aim of this study was to investigate the relationship between diabetic neuropathy and MTHFR gene C677T and 1298A ?C polymorphisms.Method
Patients with type 2 diabetes N = 248 were enrolled in the study, consisting of patients with neuropathy (N = 141) and patients without neuropathy (N = 107). MTHFR C677T polymorphism was analyzed using polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) of genomic DNA for genotyping of samples. 1298A/C polymorphism was evaluated using ARMS-PCR.Result
There was a significant difference in MTHFR polymorphism between the groups with and without neuropathy.Conclusion
Our results suggest that MTHFR 677 variant confer risk for diabetic neuropathy among Iranian patients with type 2 diabetes. 相似文献17.
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18.
Background
Nitidine chloride (NC) is known to exert anticancer and anti-metastatic effects on a variety of tumors. Recently, NC has also been shown to inhibit PIK3/AKT/mTOR axis in U87 human glioma cells.Methods
The study shows NC employing pDok2, caspase 3 dependent cell death in C6 rat glioma and U87 human malignant glioblastoma cells. The effect of NC on glioblastoma cell lines was accessed by MTT, clonogenic and wound healing assays. Cell cycle analysis was performed by FACS. Moreover, the effect of NC on downstream target proteins, such as caspase3, pDok2, PARP, and Gsk3 beta, were measured by western blotting.Results
Overexpressed pDok2 protein has recently been reported as a prognostic marker with poor outcomes for human glioblastoma multiformae. We found that NC inhibits pDok2 in U87 cells in a concentration-dependent way. We further showed that cleaved PARP and cleaved caspase 3 protein expressions were increased in C6 cells treated with NC in a dose-dependent way. NC effectively attenuated C6 cells growth and colony formation at 8 μM (micromoles) concentration. Cell cycle arrest in G2/M phase was further confirmed by flow cytometry. NC also exhibited its inhibitory effect on Gsk3 beta, which has been proven to be altered in glioma biology.Conclusions
Collectively, we predicted that NC could be employed as a potential anti-glioma mediator that needs attention to explore the mechanisms of its activity. 相似文献19.
Małgorzata Wrzosek Ada Sawicka Marek Tałałaj Marcin Wojnar Grażyna Nowicka 《Pharmacological reports : PR》2018,70(4):688-693
Background
Obesity is recognized as a major health problem. Vitamin D is involved in maintaining energy metabolism by regulation of glucose transporters, uncoupling proteins, and normal brain function. We aimed to explore a relationship between impulsivity, eating behaviors, and 25-hydroxyvitamin D concentration in a sample of 322 bariatric surgery candidates.Methods
Participants completed a questionnaire on their health, eating habits and The Eating Disorders Examination-Questionnaire (EDE-Q). Impulsivity was evaluated with the Barratt Impulsiveness Scale (BIS-11). Blood samples were obtained to measure levels of 25(OH)D, lipids (cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol), and glucose.Results
Overall scores on the BIS-11, along with scores on the Attentional Subscale of the BIS were significantly higher in participants with higher frequency of snack food consumption. Scores on the Attentional Subscale of the BIS were higher in participants who self-reported eating in response to emotions. Participants who reported eating at night or declared intense emotions associated with a desire-to-eat had the highest global, attentional, and non-planning impulsivity levels. Scores on the Non-planning Subscale of the BIS-11 were elevated in participants with 25-hydroxyvitamin D concentrations lower than 10 ng/ml.Conclusions
The results suggest that the higher level of impulsivity among the patients with obesity is associated with eating habits, and support the hypothesis that vitamin D deficiency may contribute to impulsiveness. 相似文献20.
Maria João Rodrigues Catarina Vizetto-Duarte Katkam N. Gangadhar Gokhan Zengin Adriano Mollica João Varela Luísa Barreira Luísa Custódio 《Pharmacological reports : PR》2018,70(5):896-899