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Aim To explore the effect of artesunate (ART) on the function of breast cancer cells during the progression of breast cancer and the possible mechanism of action. Methods MCF-7 (30 μmol • L-
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Aim To clarify the regulatory effect of Artesunate(ART) on tumor cell function and cell cycle in the pathological process of esophageal squamous cell carcinoma(ESCC). Methods KYSE450 and TE14 cells were treated with different concentrations of ART. The cells treated with 0 mg •L
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@#Objective To observe the effects of triptolide on drebrin and cofilin expression in the hippocampus of rats with Alzheim-er's disease (AD). Methods Sixty male Sprague-Dawley rats were equally divided into control group, model group and triptolide-treated group with 20 cases in each group. The AD model was established with unilateral injection of beta amyloid 1-40 (Aβ1- 40) into hippocampus in rats. The control group was established with unilateral injection of normal saline with the same volume into hippocampus in rats. The triptolide-treated group was administered triptolide intraperi-toneally, 0.4 mg/kg, once a day, for 15 days after modeling. Spine density of hippocampal neurons was assayed by Golgi staining. Drebrin and cofilin expression of hippocampal neurons was assayed by immunohistochemical staining and reverse transcription polymerase chain reaction (RT-PCR). Results The spine density of hippocampal neurons was higher in the triptolide-treated group than in the model group (P<0.05). The average optical density of drebrin was higher in the triptolide-treated group than in the the model group (P<0.01), while the cell number and average optical density of cofilin were lower (P<0.05). The drebrin mRNA expression was higher in the triptolide-treated group than in the model group (P<0.05), and the cofilin mRNA expression was lower (P<0.01). Conclusion Triptolide may delay the degeneration of dendritic spines in hippocampal neurons of AD rats by regulating the expression of drebrin and cofilin.
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<p><b>BACKGROUND</b>Chronic obstructive pulmonary disease (COPD) is characterized by progressive loss of lung function and local and systemic inflammation, in which CD8+ T-cells are believed to play a key role. Activated CD8+ T-cells differentiate into distinct subpopulations, including interferon-γ (IFN-γ)-producing Tc1 and interleukin (IL)-17-producing Tc17 cells. Recent evidence indicates that Tc17 cells exhibit considerable plasticity and may convert into IL-17/IFN-γ-double producing (Tc17/IFN-γ) cells when driven by inflammatory conditions. The aim of this study was to investigate the Tc17/IFN-γ subpopulation in peripheral blood of patients with COPD and to evaluate their potential roles in this disease.</p><p><b>METHODS</b>Peripheral blood samples were collected from 15 never-smokers, 23 smokers with normal lung function, and 25 patients with COPD (Global Initiative for Chronic Obstructive Lung Disease 2-4). Proportions of the IL-17/IFN-γ-double expressing subpopulation were assessed using flow cytometry. Plasma concentrations of cytokines favoring Tc17/IFN-γ differentiation were measured by enzyme-linked immunosorbent assay.</p><p><b>RESULTS</b>Patients with COPD had higher proportions of Tc17 cells and Tc17/IFN-γ cells in the peripheral blood than smokers and never-smokers. The plasticity of Tc17 cells was higher than that of Th17 cells. The percentages of Tc17 cells and Tc17/IFN-γ cells showed negative correlations with forced expiratory volume in 1 s % predicted value (r = -0.418, P = 0.03; r = -0.596, P = 0.002, respectively). The plasma concentrations of IL-6, transforming growth factor-β1, and IL-12 were significantly higher in patients with COPD compared with smokers and never-smokers.</p><p><b>CONCLUSIONS</b>Peripheral Tc17 cells are increased and more likely to convert to Tc17/IFN-γ cells in COPD, suggesting that Tc17 cell plasticity may be involved in persistent inflammation of the disease.</p>
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Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Volume Expiratório Forçado , Interferon gama , Interleucina-12 , Sangue , Interleucina-6 , Sangue , Pulmão , Doença Pulmonar Obstrutiva Crônica , Alergia e Imunologia , Células Th17 , Alergia e ImunologiaRESUMO
<p><b>OBJECTIVE</b>To observe the cytotoxicity of indirubin derivative PHII-7 against human breast cancer MCF-7 cells and to study its primary mechanisms.</p><p><b>METHODS</b>The proliferation of MCF-7 cells was detected using MTT colorimetry. Annexin V/PI double staining was applied to detect the apoptosis rate of MCF-7 cells. The distribution of cell cycles was detected using PI staining and flow cytometry (FCM). The levels of reactive oxygen species (ROS) in MCF-7 cells were detected by DCFH-DA staining. The mRNA and protein levels of c-fos were detected using RT-PCR and Westem blot analysis.</p><p><b>RESULTS</b>PHII-7 at different concentrations inhibited the proliferation of MCF-7 cells in a concentration-dependent manner, with the inhibitory rate ranging from 43.13% to 90.90% (P < 0.05). The inhibition was strengthened along with increased concentrations. PHII-7 at different concentrations could induce the apoptosis of MCF-7 cells. The early apoptosis rate was 1.43% +/- 0.02%, 9.14% +/- 0.36%, and 45.79% +/- 8.46%, respectively with the action of 1.25, 2.50, and 5.00 micromol/L PHII-7, respectively, showing dose-dependent manner. FCM analysis found that the proportion of MCF-7 cells in the G0/G1 phase and the S phase decreased after treatment with PHII-7, and the ratio of MCF-7 cells in the G2/M phase obviously increased (P < 0.01). The intra-cellular ROS level was significantly elevated 2 h after pretreatment with PHII-7. The levels of the protooncogene c-fos mRNA and protein were down-regulated in a dose-dependent manner after action of PHII-7.</p><p><b>CONCLUSIONS</b>PHII-7 exerted obvious in vitro cytotoxic effects on MCF-7 cells. Its mechanisms might be associated with arresting the cell cycle, regulating the redox equilibrium, and down-regulating the expression of the protooncogene.</p>
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Feminino , Humanos , Apoptose , Ciclo Celular , Indóis , Farmacologia , Células MCF-7RESUMO
Derived from neural stem cells (NSCs) and progenitor cells originated from the neuroectoderm, the nervous system presents an unprecedented degree of cellular diversity, interwoven to ensure correct connections for propagating information and responding to environmental cues. NSCs and progenitor cells must integrate cell-intrinsic programs and environmental cues to achieve production of appropriate types of neurons and glia at appropriate times and places during development. These developmental dynamics are reflected in changes in gene expression, which is regulated by transcription factors and at the epigenetic level. From early commitment of neural lineage to functional plasticity in terminal differentiated neurons, epigenetic regulation is involved in every step of neural development. Here we focus on the recent advance in our understanding of epigenetic regulation on orderly generation of diverse neural cell types in the mammalian nervous system, an important aspect of neural development and regenerative medicine.
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Humanos , Cromatina , Metabolismo , Metilação de DNA , Epigenômica , Histonas , Genética , Metabolismo , Células-Tronco Neurais , Biologia Celular , Metabolismo , Neurogênese , Neuroglia , Biologia Celular , Metabolismo , RNA não Traduzido , MetabolismoRESUMO
<p><b>AIM</b>To study the effect of melatonin on the induction of LTP in CA3 area of hippocampus and to investigated its possible mechanisms.</p><p><b>METHODS</b>Melatonin and other drugs (Tacrine or DNQX) were microinjected into the CA3 area. By using extracellular electrophysiological recordings to observe the changes of the slope of fEPSP in the CA3 area.</p><p><b>RESULTS</b>(1) Evoked potential and the induction of LTP were depressed by different concentration of melatonin (0.2 microg/microl, 1 microg/microl and 5 microg/microl). As the melatonin concentration increased, the induction of LTP was blocked more obviously. (2) Melatonin could attenuate the excitation effect of Tacrine (inhibitor of AChE) on LTP. (3) Inhibition of the melatonin-induced on LTP attenuated by DNQX.</p><p><b>CONCLUSION</b>The application of melatonin in rats inhibits the induction of LTP in the hippocampal CA3 area. The action of melatonin on the induction of LTP may be through the modulation of not only non-NMDA receptors but also cholinergic system.</p>
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Animais , Masculino , Ratos , Região CA3 Hipocampal , Fisiologia , Estimulação Elétrica , Potenciação de Longa Duração , Melatonina , Farmacologia , Ratos Sprague-DawleyRESUMO
<p><b>AIM</b>To investigate the influence of platelet-activating factor (PAF) receptor on long-term potentiation (LTP) attenuated by aluminium.</p><p><b>METHODS</b>The method of extracellular recording was used to investigate the effect of PAF receptors on PP-CA3 LTP by microinjection of PAF receptor antagonist Ginkgolide B or agonist mc-PAF into CA3 area.</p><p><b>RESULTS</b>(1) Amplitude of population spikes (PS) of evoked potential was not affected but LTP induction was blocked by 0.2 micromol/L ginkgolide B in CA3 area. (2) LTP induction was not influenced by 0.25 mol/L aluminium chloride, however, it could be blocked when aluminium was applicated with ginkgolide B. (3) LTP induction was influenced slightly by 40 micromol/L mc-PAF but it has no difference in statistic. LTP induction could be blocked completely by 0.5 mol/L aluminium, but when aluminium was coapplicated with mc-PAF, this effect could be relieved.</p><p><b>CONCLUSION</b>These results indicate that PAF receptors are involved in induction of LTP in CA3 area by stimulating perforant path. The inhibitory effect of aluminium on LTP is partly related to PAF receptors.</p>
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Animais , Ratos , Compostos de Alumínio , Toxicidade , Região CA3 Hipocampal , Metabolismo , Estimulação Elétrica , Potenciais Evocados , Ginkgolídeos , Farmacologia , Lactonas , Farmacologia , Potenciação de Longa Duração , Via Perfurante , Glicoproteínas da Membrana de Plaquetas , Metabolismo , Ratos Sprague-Dawley , Receptores Acoplados a Proteínas G , MetabolismoRESUMO
<p><b>OBJECTIVE</b>To evaluate the value of C-reactive protein (CRP) to diagnostic test in elderly patients with infections.</p><p><b>METHODS</b>C-reactive protein were investigated in 142 elderly patients with infections and 216 elderly patients without. CRP 7 - 20, 21 - 40 and 41 - 60 mg/L were stratified, the index of diagnostic test counted.</p><p><b>RESULTS</b>Concentrations of CRP in patients with different diseases were upper respiratory tract infection 36.9 mg/L +/- 28.9 mg/L, acute bronchitis 30.1 mg/L +/- 28.1 mg/L, pneumonia 55.9 mg/L +/- 32.9 mg/L, urinary infection 49.0 mg/L +/- 27.6 mg/L and enteritis 39.3 mg/L +/- 35.6 mg/L. They were all higher than those in control group (5.2 mg/L +/- 2.9 mg/L, P < 0.001). Stratified analysis disclosed that the specificity of CRP was 83.3% - 99.0% for diagnostic infection disease. The positive likelihood ratio (LR) of 7 - 20, 21 - 40 and 41 - 60 mg/L were 3.6, 27.0 and 128.0, respectively.</p><p><b>CONCLUSION</b>C-reactive protein was an important marker to diagnose elderly patients with infections.</p>