共查询到20条相似文献，搜索用时 31 毫秒
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Yoshihiro Nakatsu Fumio Nakagawa Sen Higashi Tomoko Ohsumi Shunji Shiiba Seiji Watanabe Hiroshi Takeuchi 《Pharmacological reports : PR》2018,70(1):29-36
Background
N-acetyl-p-aminophenol (APAP, acetaminophen, paracetamol) is a widely used analgesic/antipyretic with weak inhibitory effects on cyclooxygenase (COX) compared to non-steroidal anti-inflammatory drugs (NSAIDs). The mechanism of action of APAP is mediated by its metabolite that activates transient receptor potential channels, including transient receptor potential vanilloid 1 (TRPV1) and TRP ankyrin 1 (TRPA1) or the cannabinoid receptor type 1 (CB1). However, the exact molecular mechanism and target underlying the cellular actions of APAP remain unclear. Therefore, we investigated the effect of APAP on osteoblastic differentiation and cell migration, with a particular focus on TRP channels and CB1.Methods
Effects of APAP on osteoblastic differentiation and cell migration of MC3T3-E1, a mouse pre-osteoblast cell line, were assessed by the increase in alkaline phosphatase (ALP) activity, and both wound-healing and transwell-migration assays, respectively.Results
APAP dose-dependently inhibited osteoblastic differentiation, which was well correlated with the effects on COX activity compared with other NSAIDs. In contrast, cell migration was promoted by APAP, and this effect was not correlated with COX inhibition. None of the agonists or antagonists of TRP channels and the CB receptor affected the APAP-induced cell migration, while the effect of APAP on cell migration was abolished by down-regulating TRPV4 gene expression.Conclusion
APAP inhibited osteoblastic differentiation via COX inactivation while it promoted cell migration independently of previously known targets such as COX, TRPV1, TRPA1 channels, and CB receptors, but through the mechanism involving TRPV4. APAP may have still unidentified molecular targets that modify cellular functions. 相似文献4.
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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6.
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
Background
Juncunol is a phenanthrene isolated from the halophyte species Juncus acutus, with selective cytotoxic activity towards human hepatocarcinoma (HepG2) cells. However, its mechanism of action is unknown.Methods
The in vitro cytotoxic mechanism of juncunol was evaluated on HepG2 cells through several methods to elucidate its potential to induce apoptotic features, decrease mitochondrial membrane potential, promote internal ROS production and influence cell cycle. We also report its haemolytic activity on human erythrocytes and in silico DNA-binding studies.Results
Juncunol induced an increase in the number of apoptotic cells in a concentration-dependent manner, accompanied by a decrease in the mitochondrial membrane potential. No significant differences were observed in production of reactive oxygen species (ROS). Moreover, juncunol application at the IC50 value significantly induced cell cycle arrest in the G0/G1 phase comparatively to the control group. No significant haemolysis was detected. In silico studies indicate that juncunol seems to bind between GC base pairs.Conclusion
Juncunol reduced HepG2 cells proliferation through the induction of apoptotic cellular death, in a concentration-dependent manner. Apoptosis induction seems to be related with a decrease of the mitochondrial membrane potential but not with ROS production. Juncunol had no haemolytic activity and may act as a DNA intercalator. Our data suggests juncunol as a suitable candidate for more detailed studies, including in vivo experiments, in order to completely characterize its mode of action. 相似文献7.
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8.
Artur Beberok Dorota Wrześniok Aldona Minecka Jakub Rok Marcin Delijewski Zuzanna Rzepka Michalina Respondek Ewa Buszman 《Pharmacological reports : PR》2018,70(1):6-13
Background
Low effectiveness of anti-melanoma therapies makes it necessary to search for new drugs that could improve or replace the standard chemotherapy. Fluoroquinolones are a group of synthetic antibiotics, used in the treatment of wide range of bacterial infections. Moreover, this class of antibiotics has shown promising anti-tumor activity in several cancer cell lines. The aim of this study was to examine the effect of ciprofloxacin on cell viability, apoptosis and cell cycle distribution in COLO829 melanoma cells.Methods
Cell viability was evaluated by the WST-1 assay. Cell cycle distribution and apoptosis in cells exposed to ciprofloxacin was analyzed by the use of fluorescence image cytometer NucleoCounter NC-3000.Results
Ciprofloxacin decreased the cell viability in a dose- and time-dependent manner. For COLO829 cells treated with ciprofloxacin for 24?h, 48?h and 72?h the values of IC50 were found to be 0.74?mM, 0.17?mM and 0.10?mM, respectively. The oligonucleosomal DNA fragmentation was observed when the cells were exposed to ciprofloxacin in concentration of 1.0?mM for 48?h and 72?h. At lower ciprofloxacin concentrations (0.01?mM and 0.1?mM) cells were arrested in S-phase suggesting a mechanism related to topoisomerase II inhibition. Moreover, it was demonstrated that ciprofloxacin induced apoptosis as a result of mitochondrial membrane breakdown.Conclusions
The obtained results for COLO829 melanoma cells were compared with data for normal dark pigmented melanocytes and the use of ciprofloxacin as a potential anticancer drug for the treatment of melanoma in vivo was considered. 相似文献9.
Alina Sesarman Lucia Tefas Bianca Sylvester Emilia Licarete Valentin Rauca Lavinia Luput Laura Patras Manuela Banciu Alina Porfire 《Pharmacological reports : PR》2018,70(2):331-339
Background
Emerging treatment options for colon cancer are needed to overcome the limitations regarding the side effects of current chemotherapeutics and drug resistance. The goal of this study was to assess the antitumor actions of PEGylated long-circulating liposomes (LCL) co-delivering curcumin (CURC) and doxorubicin (DOX) on murine colon carcinoma cells (C26).Methods
The cytotoxicity of CURC and DOX, administered alone or in combination, either in free or LCL form, was evaluated with regard to antiproliferative effects on C26 cells and to protumor processes that might be affected.Results
Our results indicated that PEGylated LCL-CURC-DOX exerted strong antiproliferative effects on C26 cells, slightly exceeding those induced by free CURC-DOX, but higher than either agent administered alone in their free form. These effects of LCL-CURC-DOX were due to the inhibition of the production of angiogenic/inflammatory proteins in a NF-κB-dependent manner, but were independent of ROS production or AP-1 c-Jun activation. Notable, the anti-angiogenic actions of LCL-CURC-DOX appeared to be much stronger than those induced by the co-administration of CURC and DOX in their free form, on C26 colon cancer cells.Conclusion
LCL-CURC-DOX demonstrated enhanced cytotoxicity on C26 murine colon cancer cells by inhibiting the production of the majority of factors involved in tumor-associated angiogenesis and inflammation and is now being evaluated in vivo regarding its efficacy towards tumor growth in colon cancer. 相似文献10.
Elvia Mena-Avila Ricardo Márquez-Gómez Guillermo Aquino-Miranda Gustavo Nieto-Alamilla José-Antonio Arias-Montaño 《Pharmacological reports : PR》2018,70(1):146-155
Background
Clobenpropit, a potent antagonist/inverse agonist at the histamine H3 receptor (H3R), reduced the cytotoxic action of 6-hydroxydopamine (6-OHDA) in neuroblastoma SH-SY5Y cells transfected with the human H3R. We therefore set out to study whether this effect involved a receptor-independent action on dopamine transport.Methods
The uptake of [3H]-dopamine was assayed in SH-SY5Y cells and rat striatal or cerebro-cortical isolated nerve terminals (synaptosomes). Clobenpropit binding to the human norepinephrine (NET) and dopamine (DAT) transporters was analyzed by molecular modeling.Results
In SH-SY5Y cells, [3H]-dopamine uptake was inhibited by desipramine (selective NET inhibitor), GBR-12909 (selective DAT inhibitor), and fluoxetine (selective inhibitor of the serotonin transporter, SERT) with IC50 values 37, 537, and 2800 nM, respectively. The potency rank order indicates that [3H]-dopamine uptake is primarily performed by NET. Clobenpropit inhibited [3H]-dopamine uptake (maximum inhibition 82.7 ± 2.8%, IC50 490 nM), and the effect was reproduced by the H3R antagonist/inverse agonist iodophenpropit, but not by the agonists R-α-methylhistamine and immepip or the antagonists/inverse agonists ciproxifan and A-331440. Clobenpropit also inhibited [3H]-dopamine uptake by rat striatal and cerebro-cortical synaptosomes (?54.6 ± 11.3% and ?46.3 ± 9.6%, respectively, at 10 μM). Modeling of the human NET and DAT obtained by homology from the crystal of Drosophila melanogaster DAT showed that clobenpropit can bind to a site also recognized in both transporters by nisoxetine, a potent NET inhibitor.Conclusion
These data indicate a direct inhibitory effect of clobenpropit on catecholamine transport. 相似文献11.
Maksym V. Kopanitsa Gemma Gou Nurudeen O. Afinowi Àlex Bayés Seth G.N. Grant Noboru H. Komiyama 《Pharmacological reports : PR》2018,70(4):777-783
Background
Synaptic Ras-GTPase-activating protein 1 (SYNGAP1) is an abundant brain-specific protein localized at the postsynaptic density of mammalian excitatory synapses. SYNGAP1 functions as a crucial regulator of downstream intracellular signaling triggered by N-methyl-d-aspartate receptor activation. One of the most important signaling pathways regulated by SYNGAP1 is the Ras-Raf-MEK-ERK pathway. SYNGAP1 deficiency is associated with hyperphosphorylation of MEK and ERK kinases and with altered synaptic function in Syngap1+/? mice. Loss-of-function mutations in the SYNGAP1 gene have been documented in many human cognitive and neurological disorders. However, there are currently no approaches that reverse the phenotypes of SYNGAP1 deficiency.Methods
Using electrophysiological recordings of field responses in hippocampal slices, we examined if disturbances of synaptic physiology in the hippocampus of 7–8-month old Syngap1+/? mice were sensitive to the effect of the MEK inhibitor PD-0325901 given orally for 6 days.Results
We found that in hippocampal slices from vehicle-treated Syngap1+/? mice, basal synaptic responses were higher and their long-term potentiation (LTP) was lower than in slices from wild-type littermates. Chronic administration of PD-0325901 normalized basal synaptic responses, but did not reverse LTP deficit.Conclusions
The differential sensitivity of basal synaptic transmission and LTP to MEK inhibition indicates that the effects of SYNGAP1 deficiency on these synaptic parameters are mediated by distinct pathways. Our findings also suggest that at least some physiological phenotypes of the germline Syngap1 mutation can be ameliorated by pharmacological treatment of adult animals. 相似文献12.
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13.
Chan Chen Yan-hua Li Qiong Zhang Jie-zhong Yu Yong-fei Zhao Cun-gen Ma Bao-guo Xiao 《Acta pharmacologica Sinica》2014,35(11):1428-1438
Aim:
Fasudil, a selective Rho kinase (ROCK) inhibitor, has been shown to alleviate the severity of experimental autoimmune encephalomyelitis (EAE) via attenuating demyelination and neuroinflammation. The aim of this study was to investigate the effects of fasudil on interactions between macrophages/microglia and T cells in a mice EAE model.Methods:
Mouse BV-2 microglia were treated with IFN-γ and fasudil. Cell viability was detected with MTT assay. BV-2 microglia polarization was analyzed using flow cytometry. Cytokines and other proteins were detected with ELISA and Western blotting, respectively. Mice were immunized with MOG35–55 to induce EAE, and then treated with fasudil (40 mg/kg, ip) every other day from d 3 to d 27 pi. Encephalomyelitic T cells were prepared from the spleen of mice immunized with MOG35–55 on d 9 pi.Results:
Treatment of mouse BV-2 microglia with fasudil (15 μg/mL) induced significant phenotype polarization and functional plasticity, shifting M1 to M2 polarization. When co-cultured with the encephalomyelitic T cells, fasudil-treated BV-2 microglia significantly inhibited the proliferation of antigen-reactive T cells, and down-regulated IL-17-expressing CD4+ T cells and IL-17 production. Furthermore, fasudil-treated BV-2 microglia significantly up-regulated CD4+CD25high and CD4+IL-10+ regulatory T cells (Tregs) and IL-10 production, suggesting that the encephalomyelitic T cells had converted to Tregs. In EAE mice, fasudil administration significantly decreased both CD11b+iNOS+ and CD11b+TNF-α+ M1 microglia, and increased CD11b+IL-10+ M2 microglia.Conclusion:
Fasudil polarizes BV-2 microglia into M2 cells, which convert the encephalomyelitic T cells into Tregs in the mice EAE model. 相似文献14.
Faisal Imam Naif O. Al-Harbi Mohammad Matar Al-Harbi Mushtaq Ahmad Ansari Abdullah F Al-Asmari Mohd Nazam Ansari Wael A. Al-Anazi Saleh Bahashwan Mashal M Almutairi Musaad Alshammari Mohammad Rashid Khan Abdulaziz Mohammed Alsaad Moureq Rashed Alotaibi 《Pharmacological reports : PR》2018,70(5):993-1000
Background
Doxorubicin is an effective, potent and commonly used anthracycline-related anticancer drug; however, cardiotoxicity compromises its therapeutic potential. Apremilast, a novel phosphodiesterase type 4-inhibitor, reported to have anti-inflammatory effects and modulating many inflammatory mediators.Methods
The present study investigated the influence of apremilast against doxorubicin-induced cardiotoxicity in male Wistar rats. A total, 24 animals were divided into four groups of six animal each. Group 1, served as control and received normal saline. Group 2 animals, received doxorubicin (20 mg kg?1, ip). Group 3 and 4, treatment group, received doxorubicin (20 mg kg?1, ip) with the same schedule as group-2, plus apremilast (10 and 20 mg kg?1 day?1, po) respectively. Oxidative stress, caspase-3 enzyme activity, gene expression and protein expression were tested.Results
The results of the present study demonstrated that administration of apremilast reversed doxorubicin-induced cardiotoxicity.Conclusion
These findings suggested that apremilast can attenuate doxorubicin-induced cardiotoxicity via inhibition of oxidative stress mediated activation of nuclear factor-kappa B signaling pathways. 相似文献15.
Protective effects of curcumin on acrolein-induced neurotoxicity in HT22 mouse hippocampal cells 总被引：1，自引：0，他引：1
Lan-Ying Shi Li Zhang Hui Li Tao-Li Liu Ji-Cai Lai Zhi-Bing Wu Jian Qin 《Pharmacological reports : PR》2018,70(5):1040-1046
Background
Aging is one of the most important inevitable risk factors of Alzheimer disease (AD). Oxidative stress plays a critical role in the process of aging. Curcumin has been proposed to improve neural damage, especially neurodegenerative injury, through its antioxidant and anti-inflammatory properties. Therefore, we investigated the effects of curcumin on acrolein-induced AD-like pathologies in HT22 cells.Methods
HT22 murine hippocampal neuronal cells were treated with 25 μM acrolein for 24 h with or without pre-treating with curcumin at the selected optimum concentration (5 μg/mL) for 30 min. Cell viability and apoptosis were measured by CCK8 assay and flow cytometric analysis. Levels of glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) were detected by a GSH assay kit or commercial assay kits, respectively. Alterations in the expression of BDNF/TrkB and key enzymes involved in amyloid precursor protein (APP) metabolism were assessed by western blotting.Results
Data showed that curcumin significantly reversed acrolein-induced oxidative stress indicated by depletion of GSH and SOD, and elevation of MDA. The findings also suggested curcumin’s potential in protecting HT22 cells against acrolein through regulating the BDNF/TrkB signaling. In addition, acrolein-induced reduction in A-disintegrin and metalloprotease, and the increase of amyloid precursor protein, β-secretase, and receptor for advanced glycation end products were reversed either, and most of them were nearly restored to the control levels by curcumin.Conclusion
These findings demonstrate the protective effects of curcumin on acrolein-induced neurotoxicity in vitro, which further suggests its potential role in the treatment of AD. 相似文献16.
Yueh-Lun Lee Ling-Heng Hsu Yueh-Hsiung Kuo Chen-Chen Lee 《Pharmacological reports : PR》2019,71(2):194-200
Background
Caffeic amides are derivatives of caffeic acid, which have antioxidant and anti-inflammatory properties, and high in vivo stability. The therapeutic effect of caffeic amides on allergic diseases, and especially on the maturation of bone marrow-derived dendritic cells (BM-DCs), remains unclear. In this study, we investigated the therapeutic potential of caffeic amides on allergic diseases by evaluating the maturation of DCs and evaluated their potential in inducing the differentiation of TH2 cells.Methods
BM-DCs isolated from BALB/c mice were treated with different caffeic amide derivatives for 48?h and the expression of surface markers was analyzed by flow cytometry. The differentiation of CD4+ T cells was detected by the 5-bromo-2-deoxyuridine (BrdU) incorporation assay and cytokine production was analyzed by ELISA.Results
Our results showed that among the six caffeic amides tested herein, only 36?M significantly inhibited the antigen-induced maturation of DCs associated with the expression of CD80, CD86, and major histocompatibility complex II (VC ovalbumin (OVA)+ thymic stromal lymphopoietin (TSLP) vs. 36?M OVA?+?TSLP). Additionally, the isolation and co-culture of antigen-specific CD4+ T cells with 36?M-treated BM-DCs suppressed the antigen-specific differentiation of TH2 cells.Conclusion
Among the six caffeic amides tested herein, 36?M (N-octyl caffeamide) might possess therapeutic potential for allergic diseases. 相似文献17.
Yuichiro Amano Hiroko Yamakawa Kazuko Yonemori Mitsuyuki Shimada Ryuichi Tozawa 《Pharmacological reports : PR》2018,70(1):172-177
Background
The effects of farnesoid X receptor (FXR) antagonists on plasma lipid profile in mice have not been investigated thus far. The aim of this study was to investigate the antidyslipidemic effects of an FXR antagonist in dyslipidemic mice, and to clarify the mechanisms underlying the lipid modulatory effect.Methods
Compound-T0 (1–100?mg/kg) was orally administered to C57BL/6J mice fed a Western-type diet or low-density lipoprotein receptor knockout (LDLR-/-) mice fed a Western-type diet for a week, and plasma lipid levels were investigated. Effects on lipid clearance, hepatic triglyceride secretion after Triton WR-1339 challenge, and intestinal lipid absorption were investigated after multiple dosing.Results
Compound-T0 significantly increased plasma level of non-high-density lipoprotein cholesterol in both C57BL/6 and LDLR-/- mice; in addition, it significantly increased plasma triglyceride level in LDLR-/- mice. Compound-T0 failed to enhance the clearance of 3,3′-dioctadecylindocarbocyanine (DiI)-labeled LDL in C57BL/6J mice. Although compound-T0 did not affect triglyceride clearance and hepatic triglyceride secretion, it significantly increased intestinal [3H]cholesterol absorption in LDLR-/- mice.Conclusions
It was found that the FXR antagonist, compound-T0 exacerbated dyslipidemia in mice because it enhanced intestinal lipid absorption via acceleration of bile acid excretion. 相似文献18.
Background
Bardoxolone methyl (RTA 402, CDDOMe) has been long known for its anti-inflammatory and exceptional cytotoxic activity. The biological responses to CDDOMe are truly dose dependent. And owing to the structural modifications introduced in its parent molecule oleanolic acid, CDDOMe is able to form reversible adducts with cellular proteins containing redox sensitive cysteine residues. This nature of CDDOMe makes it a multifunctional molecule targeting multiple signaling pathways. This study was initiated to study the response of Neuro2a, a mouse neuroblastoma cell line to CDDOMe.Methods
Neuro2a cells were treated with CDDOMe and all trans retinoic acid (ATRA) for 4 days and observed for neurite outgrowth. The neurite length was estimated using ImageJ software (Neuron growth plugin). Cell viability was investigated using MTT dye reduction and trypan blue dye exclusion method. Gene expression of differentiation markers was analyzed using quantitative PCR. Cellular localization of Tuj1 and synaptophysin in differentiated Neuro2a cells was observed using immunofluorescence.Results
CDDOMe ceased proliferation and induced dramatic neurite outgrowth in Neuro2a cells. These morphological changes were accompanied by time dependent increase in the mRNA levels of tyrosine hydroxylase, neurofilament 200 and synaptophysin. Besides, cytoskeleton protein Tuj1 and the synaptic vesicle protein synaptophysin were also observed to be localized in the neurites induced by CDDOMe.Conclusions
These early shreds of evidence suggest that CDDOMe induces differentiation in Neuro2a cells at concentrations ranging from 0.2 to 0.4 μM and indeed contributes the existing knowledge on CDDOMe induced activities in cells. 相似文献19.
Maria Skibinska Agata Groszewska Pawel Kapelski Aleksandra Rajewska-Rager Joanna Pawlak Monika Dmitrzak-Weglarz Aleksandra Szczepankiewicz Joanna Twarowska-Hauser 《Pharmacological reports : PR》2018,70(1):55-59