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1.
J Integr Neurosci ; 18(3): 237-243, 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31601071

RESUMO

Low-frequency repetitive transcranial magnetic stimulation (rTMS) has been considered as a treatment option for depression and anxiety. However, its role in epilepsy comorbid with depression and anxiety is unclear. Therefore, we evaluated whether low-frequency rTMS can alleviate depression- and anxiety-like behavior in epileptic rats. Forty-eight adult rats were allocated at random to four groups: Control, Pentylenetetrazol (PTZ), PTZ-rTMS and PTZ-Sham. The control group received intraperitoneal injections of normal saline, while the other groups received intraperitoneal injections of pentylenetetrazol (35 mg/kg/d) once a day for 15 days. Low-frequency rTMS or sham stimulation were administered to the PTZ-rTMS and PTZ-Sham group, respectively, over the two-week period. The open-field test (OFT), elevated plus-maze test (EPM) and forced swimming test (FST) were carried out before the experiment, on the 8th and 15th day to assess depression- and anxiety-like behavior in the rats. Two weeks of low-frequency rTMS treatment could not impair the increases of seizure severity in epileptic rats. However, relative to the PTZ and PTZ-Sham group, the two-week low-frequency rTMS treatment significantly reduced the immobility time in the forced swimming test and attenuated the progressive decrease in total distance traveled, frequency of rearing, velocity in the open-field test, number of entries in the open arms (%) and the time spent in the open arms (%) in the elevated plus-maze test of the PTZ-rTMS group. We proposed that low-frequency rTMS can benefit epileptic rats via amelioration of comorbid depression and anxiety, but it can not alleviate the seizure severity.

2.
Artigo em Inglês | MEDLINE | ID: mdl-31553228

RESUMO

Objective: Toutongning (TTN) capsule, a Chinese patent medicine, is used as a prophylactic treatment for migraine. The present study was conducted as a postmarketing evaluation of the efficacy and safety of TTN capsule. Design: A randomized, double-blind, placebo-controlled trial. Location: Patients recruited from 14 medical centers in China from May 2014 to August 2015. Subjects: Patients between 18 and 65 years of age with a diagnosis of migraine. Interventions: The patients were randomly assigned to receive either TTN (1200 mg, three times daily) or a matched placebo (1:1) for 4 weeks. Outcome measures: The primary outcome measured was a minimum 50% reduction in the frequency of headaches from the 4-week baseline period to the last 4 weeks of the 12-week trial. Secondary outcomes included duration, days, and visual analog score of headache attack, interval between headache attacks, usage of acute analgesics, and score on the Headache Impact Test-6. In addition, all patients were evaluated for adverse events (AEs). Results: This study initially enrolled 400 patients; a total of 378 participants completed the experiment while fulfilling all study requirements. TTN had a superior effect compared with the placebo on both the primary and secondary outcome measures without any serious AEs or unexpected side effects. Conclusion: TTN can effectively prevent the occurrence of migraine headaches and is well-tolerated and safe. TTN may exhibit a persistent therapeutic effect even after cessation of use. Trial Registration number: ChiCTR-IPR-15007058.

3.
Cell Prolif ; 52(5): e12665, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31332862

RESUMO

OBJECTIVES: Abnormal activation of NF-κB signalling is a major mechanism of apoptosis resistance in glioblastoma multiforme (GBM). Therefore, better understanding of the regulation of NF-κB signalling has a significant impact for GBM therapy. Here, we uncovered a critical role of the small GTPase RND3 in regulating the p65 subunit of NF-κB and NF-κB signalling in GBM. MATERIALS AND METHODS: Human GBM samples, GBM cells and a human orthotopic GBM-xenografted animal model were used. The mechanisms of RND3 in regulation of NF-κB signalling and GBM cell apoptosis were examined by luciferase assay, quantitative PCR, immunostaining, immunoblotting, immunofluorescence, coimmunoprecipitation, TUNEL staining, JC-1 analysis and flow cytometry. RESULTS: Overexpression of RND3 led to reduced p65 activity in GBM-cultured cells and a GBM animal model, indicating that the NF-κB pathway is negatively regulated by RND3 in GBM. Mechanistically, we found that RND3 bound p65 and promoted p65 ubiquitination, leading to decreased p65 protein levels. Furthermore, RND3 enhanced cleaved caspase 3 levels and promoted apoptosis in GBM cells, and RND3 expression was positively correlated with cleaved caspase 3 and IL-8 in human GBM samples. The effect of RND3 on promoting apoptosis disappeared when p65 ubiquitination was blocked by protease inhibitor carfilzomib or upon co-expression of ectopic p65. CONCLUSIONS: RND3 binds p65 protein and promotes its ubiquitination, resulting in reduced p65 protein expression and inhibition of NF-κB signalling to induce GBM cell apoptosis.


Assuntos
Neoplasias Encefálicas/patologia , Glioblastoma/patologia , Transdução de Sinais , Proteínas rho de Ligação ao GTP/metabolismo , Animais , Apoptose/efeitos dos fármacos , Neoplasias Encefálicas/metabolismo , Caspase 3/metabolismo , Linhagem Celular Tumoral , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Glioblastoma/metabolismo , Humanos , Interleucina-8/metabolismo , Camundongos , Camundongos Nus , Oligopeptídeos/farmacologia , Ligação Proteica , Transdução de Sinais/efeitos dos fármacos , Fator de Transcrição RelA/genética , Fator de Transcrição RelA/metabolismo , Transplante Heterólogo , Ubiquitinação/efeitos dos fármacos , Proteínas rho de Ligação ao GTP/genética
4.
Psychiatry Res ; 271: 52-59, 2018 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-30469089

RESUMO

Depressive and anxiety symptoms are frequently observed in breast cancer survivors. To date, few randomized controlled trials have been conducted on the efficacy of cognitive behavioural therapy (CBT) for depressive and anxiety symptoms in Chinese population. This study aims to verify the efficacy of CBT in Chinese breast cancer survivors. Women (n = 392) with breast cancer were randomly assigned to 3 groups: CBT (n = 98), self-care management (SCM, n = 98), and usual care (UC, n = 196) using the proportion 1:1:2. Women in the CBT and SCM groups received a series of nine sessions for 12 weeks, while women in the UC group received their usual medical care only. Depressive and anxiety symptoms were assessed using the Hamilton Depression Rating Scale (HAMD) and the Hamilton Anxiety Scale (HAMA) score at baseline, 2, 4, 8, 12, 16, and 24 weeks. A significant intergroup difference was found in the HAMD and HAMA scores. Women in the CBT group showed significantly less depressive and anxiety symptoms compared with women in the SCM and UC groups over time. In conclusion, this study supports the efficacy of CBT for depressive and anxiety symptoms in Chinese breast cancer survivors.

5.
Neuropsychiatr Dis Treat ; 14: 2665-2673, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30349264

RESUMO

Purpose: Cognitive behavioral therapy (CBT) for depression had been found to be effective in reducing depressive and anxiety symptoms in breast cancer survivors. It is not known whether CBT for depression would also improve insomnia and quality of life (QOL). The aim of this study was to investigate whether CBT for depression would improve insomnia and QOL in a randomized controlled multicenter trial. Patients and methods: In this study, breast cancer survivors (n=392) were randomly allocated to the following three groups: CBT (n=98), self-care management (SCM, n=98), and usual care (UC, n=196) in a ratio of 1:1:2. CBT and SCM received a series of nine sessions for 12 weeks, whereas UC received UC only. Insomnia and QOL were evaluated using Athens Insomnia Scale (AIS) and Functional Assessment of Cancer Therapy-Breast (FACT-B) questionnaire at baseline, 4, 12, and 24 weeks. Results: There was a significant intergroup difference in AIS and FACT-B scores (both P<0.01). CBT showed less insomnia problems and better overall QOL compared with those in SCM and UC (both P<0.01). No significant differences were found between SCM and UC in insomnia problems and overall QOL. Moreover, the effects of CBT on insomnia and QOL were maintained during the follow-up period. Conclusion: CBT for depression can be effective in improving insomnia problems and QOL in the Chinese breast cancer survivors.

6.
Artigo em Inglês | MEDLINE | ID: mdl-29859854

RESUMO

BACKGROUND: Observational studies, including recent large cohort studies, have reported an association between depression and the risk of Parkinson's disease (PD); however, conclusions were inconsistent. Clarifying this relation might improve the understanding of risk factors for and the disease mechanisms in PD. Therefore, we performed a meta-analysis to examine whether depression is associated with an increased risk of PD. METHODS: A literature search in the PubMed, EMBASE, Scopus, PsycINFO and Web of Science databases was undertaken through March 2018, looking for observational studies evaluating the association between depression and the risk of PD. Pooled relative risk (RR) estimates and 95% confidence intervals (CIs) were calculated using a random-effects model. Subgroup analyses and sensitivity analyses were also performed. RESULTS: A random-effects meta-analysis of 5 cohort studies and 6 case-control studies demonstrated a significant positive association between depression and a subsequent risk of PD (RR, 2.20; 95% CI, 1.87-2.58), and it was consistent across subgroups. Furthermore, sensitivity analysis confirmed the stability of the results; visual examination of funnel plots and Begg's and Egger's tests showed no evidence of publication bias. CONCLUSIONS: Our meta-analysis demonstrated that persons with depression exhibited an increased risk of a subsequent PD diagnosis. The pathophysiological and psychological mechanisms underlying this association are still unclear and warrant further research.

7.
Oncotarget ; 8(53): 91112-91122, 2017 Oct 31.
Artigo em Inglês | MEDLINE | ID: mdl-29207629

RESUMO

Rnd3, a Rho GTPase, is involved in the inhibition of actin cytoskeleton dynamics through the Rho kinase-dependent signaling pathway. We previously demonstrated that mice with genetic deletion of Rnd3 developed a markedly larger brain compared with wild-type mice. Here, we demonstrate that Rnd3 knockout mice developed an enlarged subventricular zone, and we identify a novel role for Rnd3 as an inhibitor of Notch signaling in neural stem cells. Rnd3 deficiency, both in vivo and in vitro, resulted in increased levels of Notch intracellular domain protein. This led to enhanced Notch signaling and promotion of aberrant neural stem cell growth, thereby resulting in a larger subventricular zone and a markedly larger brain. Inhibition of Notch activity abrogated this aberrant neural stem cell growth.

8.
Neurochem Res ; 42(10): 2996-3004, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28631231

RESUMO

DNA polymerase-ß (DNA pol-ß) plays a crucial role in the pathogenesis of Parkinson's disease (PD). The aim of this study was to investigate the neuroprotective effects of a DNA polymerase-ß inhibitor 2',3'-dideoxycytidine (DDC) in PD models. In the in vitro studies, primary cultured neurons were challenged with 1-methyl-4-phenylpyridinium ion (MPP+). The expression of DNA pol-ß was assessed using western blot. The neuroprotective effect of DNA pol-ß knockdown and DNA pol-ß inhibitor DDC was determined using cell viability assay and caspase-3 activity assay. We found that MPP+ induced neuronal death and the activation of caspase-3 in a dose-dependent manner. The expression of DNA pol-ß increased after the neurons were exposed to MPP+. DNA pol-ß siRNA or DNA pol-ß inhibitor DDC attenuated neuronal death induced by MPP+. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD, MPTP treatment triggered behavioral deficits and nigrostriatal lesions. Pretreatment with DDC attenuated MPTP-induced behavioral deficits, dopaminergic neuronal death and striatal dopamine depletion in the MPTP mouse model. These results indicate that DNA pol-ß inhibitors may present a novel promising therapeutic option for the neuroprotective treatment of PD.


Assuntos
Morte Celular/efeitos dos fármacos , Dopamina/metabolismo , Neurônios Dopaminérgicos/efeitos dos fármacos , Substância Negra/efeitos dos fármacos , Zalcitabina/farmacologia , 1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina/farmacologia , Animais , Células Cultivadas , Modelos Animais de Doenças , Camundongos , Fármacos Neuroprotetores/farmacologia , Substância Negra/metabolismo
9.
Oxid Med Cell Longev ; 2017: 8495160, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29391926

RESUMO

Neurological function deficits due to cerebral ischemia or neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD) have long been considered a thorny issue in clinical treatment. Recovery after neurologic impairment is fairly limited, which poses a major threat to health and quality of life. Accumulating evidences support that ROS and autophagy are both implicated in the onset and development of neurological disorders. Notably, oxidative stress triggered by excess of ROS not only puts the brain in a vulnerable state but also enhances the virulence of other pathogenic factors, just like mitochondrial dysfunction, which is described as the culprit of nerve cell damage. Nevertheless, autophagy is proposed as a subtle cellular defense mode against destructive stimulus by timely removal of damaged and cytotoxic substance. Emerging evidence suggests that the interplay of ROS and autophagy may establish a determinant role in the modulation of neuronal homeostasis. However, the underlying regulatory mechanisms are still largely unexplored. This review sets out to afford an overview of the crosstalk between ROS and autophagy and discusses relevant molecular mechanisms in cerebral ischemia, AD, and PD, so as to provide new insights into promising therapeutic targets for the abovementioned neurological conditions.


Assuntos
Autofagia/genética , Encéfalo/patologia , Doenças do Sistema Nervoso/terapia , Espécies Reativas de Oxigênio/uso terapêutico , Humanos , Espécies Reativas de Oxigênio/farmacologia
10.
Oncotarget ; 7(50): 82411-82423, 2016 Dec 13.
Artigo em Inglês | MEDLINE | ID: mdl-27705942

RESUMO

Activation of Snail1 signaling promotes the migration and invasion of multiple tumors, including glioblastoma multiforme (GBM). However, the molecular mechanism that augments Snail1 signaling during GBM cell migration and invasion remains largely unknown. Identification of the factors that regulate Snail1 signaling is critical to block tumor cell migration and invasion. By screening human GBM specimens, we found that the expression levels of small GTPase RND3 positively correlated with the expression levels of E-cadherin and claudin, the glioblastoma migration biomarkers negatively regulated by Snail1. Downregulation of E-cadherin and claudin has been associated with the migration and invasion of GBM cells. We demonstrated that RND3 functioned as an endogenous inhibitor of the Snail-directed transcriptional regulation. RND3 physically interacted with Snail1 protein, enhanced Snail1 ubiquitination, and facilitated the protein degradation. Forced expression of RND3 inhibited Snail1 activity, which in turn blocked glioblastoma cell migration and invasion in vitro in cell culture and in vivo in GBM xenograft mice. In contrast, downregulation of RND3 augmented Snail1 activity, and subsequently decreased E-cadherin expression, eventually promoted glioblastoma cell migration and invasion. The pro-migration induced by RND3 downregulation was attenuated by Snail1 knockdown. The findings partially explain why Snail1 activity is augmented in GBM, and defines a new function of RND3 in GBM cell migration and invasion.


Assuntos
Neoplasias Encefálicas/enzimologia , Movimento Celular , Glioblastoma/enzimologia , Fatores de Transcrição da Família Snail/metabolismo , Proteínas rho de Ligação ao GTP/metabolismo , Animais , Antígenos CD , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/patologia , Caderinas/genética , Caderinas/metabolismo , Linhagem Celular Tumoral , Claudinas/genética , Claudinas/metabolismo , Regulação Neoplásica da Expressão Gênica , Glioblastoma/genética , Glioblastoma/patologia , Humanos , Masculino , Camundongos Nus , Invasividade Neoplásica , Ligação Proteica , Proteólise , Interferência de RNA , Transdução de Sinais , Fatores de Transcrição da Família Snail/genética , Transfecção , Ubiquitinação , Proteínas rho de Ligação ao GTP/genética
11.
Front Neuroanat ; 10: 54, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27242450

RESUMO

A60, the mouse monoclonal antibody against the neuronal nuclear protein (NeuN), is the most widely used neuronal marker in neuroscience research and neuropathological assays. Previous studies identified fragments of A60-immunoprecipitated protein as Synapsin I (Syn I), suggesting the antibody will demonstrate cross immunoreactivity. However, the likelihood of cross reactivity has never been verified by immunohistochemical techniques. Using our established tissue processing and immunofluorescent staining protocols, we found that A60 consistently labeled mossy fiber terminals in hippocampal area CA3. These A60-positive mossy fiber terminals could also be labeled by Syn I antibody. After treating brain slices with saponin in order to better preserve various membrane and/or vesicular proteins for immunostaining, we observed that A60 could also label additional synapses in various brain areas. Therefore, we used A60 together with a rabbit monoclonal NeuN antibody to confirm the existence of this cross reactivity. We showed that the putative band positive for A60 and Syn I could not be detected by the rabbit anti-NeuN in Western blotting. As efficient as Millipore A60 to recognize neuronal nuclei, the rabbit NeuN antibody demonstrated no labeling of synaptic structures in immunofluorescent staining. The present study successfully verified the cross reactivity present in immunohistochemistry, cautioning that A60 may not be the ideal biomarker to verify neuronal identity due to its cross immunoreactivity. In contrast, the rabbit monoclonal NeuN antibody used in this study may be a better candidate to substitute for A60.

12.
Cancer Med ; 4(9): 1404-16, 2015 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-26108681

RESUMO

Activation of Notch signaling contributes to glioblastoma multiform (GBM) tumorigenesis. However, the molecular mechanism that promotes the Notch signaling augmentation during GBM genesis remains largely unknown. Identification of new factors that regulate Notch signaling is critical for tumor treatment. The expression levels of RND3 and its clinical implication were analyzed in GBM patients. Identification of RND3 as a novel factor in GBM genesis was demonstrated in vitro by cell experiments and in vivo by a GBM xenograft model. We found that RND3 expression was significantly decreased in human glioblastoma. The levels of RND3 expression were inversely correlated with Notch activity, tumor size, and tumor cell proliferation, and positively correlated with patient survival time. We demonstrated that RND3 functioned as an endogenous repressor of the Notch transcriptional complex. RND3 physically interacted with NICD, CSL, and MAML1, the Notch transcriptional complex factors, promoted NICD ubiquitination, and facilitated the degradation of these cofactor proteins. We further revealed that RND3 facilitated the binding of NICD to FBW7, a ubiquitin ligase, and consequently enhanced NICD protein degradation. Therefore, Notch transcriptional activity was inhibited. Forced expression of RND3 repressed Notch signaling, which led to the inhibition of glioblastoma cell proliferation in vitro and tumor growth in the xenograft mice in vivo. Downregulation of RND3, however, enhanced Notch signaling activity, and subsequently promoted glioma cell proliferation. Inhibition of Notch activity abolished RND3 deficiency-mediated GBM cell proliferation. We conclude that downregulation of RND3 is responsible for the enhancement of Notch activity that promotes glioblastoma genesis.


Assuntos
Neoplasias Encefálicas/genética , Neoplasias Encefálicas/metabolismo , Transformação Celular Neoplásica/genética , Transformação Celular Neoplásica/metabolismo , Glioblastoma/genética , Glioblastoma/metabolismo , Receptores Notch/metabolismo , Proteínas rho de Ligação ao GTP/genética , Animais , Neoplasias Encefálicas/patologia , Linhagem Celular Tumoral , Proliferação de Células , Modelos Animais de Doenças , Regulação para Baixo , Regulação Neoplásica da Expressão Gênica , Glioblastoma/patologia , Xenoenxertos , Humanos , Masculino , Camundongos , Complexos Multiproteicos/metabolismo , Ligação Proteica , Proteólise , Transdução de Sinais , Ativação Transcricional , Carga Tumoral , Ubiquitinação , Proteínas rho de Ligação ao GTP/metabolismo
13.
Zhongguo Zhong Xi Yi Jie He Za Zhi ; 33(1): 27-30, 2013 Jan.
Artigo em Chinês | MEDLINE | ID: mdl-23596781

RESUMO

OBJECTIVE: To observe early intervention effects of Modified Shuyu Pill (MSP) on vascular cognitive impairment no dementia (VCIND). METHODS: Totally 100 patients VCIND were randomly assigned to the treatment group (43 cases) and the control group (33 cases). On the basis of the treatment targeting risk factors of blood vessels, patients in the treatment group were treated by MSP, while those in the control group were treated by donepezil hydrochloride. The therapeutic course was 16 weeks. The neuropsychological scales [mini-mental state examination (MMSE) and Montreal cognitive assessment (MOCA) score] and Chinese medicine dementia syndromes scales were observed before and after treatment. RESULTS: The MMSE and MOCA score of the two groups increased when compared with the same group before treatment (P < 0.01). But there was no statistical difference in MMSE or MOCA score after treatment between the two groups (P > 0.05). The Chinese medicine dementia syndromes scales significantly decreased in the treatment group when compared with before treatment (P < 0.01). But there was no statistical difference in Chinese medicine dementia syndromes scales in the control group between before and after treatment (P > 0.05). There was statistical difference in Chinese medicine dementia syndromes scales after treatment between the two groups (P < 0.01). CONCLUSION: MSP could effectively intervene the progress of VCIND.


Assuntos
Transtornos Cognitivos/prevenção & controle , Medicamentos de Ervas Chinesas/uso terapêutico , Intervenção Médica Precoce , Idoso , Donepezila , Feminino , Humanos , Indanos/uso terapêutico , Masculino , Pessoa de Meia-Idade , Piperidinas/uso terapêutico
14.
J Chem Theory Comput ; 9(1): 263-72, 2013 Jan 08.
Artigo em Inglês | MEDLINE | ID: mdl-26589028

RESUMO

By incorporating the improved empirical atom-atom dispersion corrections from DFT-D3 [Grimme, S.; Antony, J.; Ehrlich, S.; Krieg, H. J. Chem. Phys.2010, 132, 154104], two long-range corrected (LC) hybrid density functionals are proposed. Our resulting LC hybrid functionals, ωM06-D3 and ωB97X-D3, are shown to be accurate for a very wide range of applications, such as thermochemistry, kinetics, noncovalent interactions, frontier orbital energies, fundamental gaps, and long-range charge-transfer excitations, when compared with common global and LC hybrid functionals. Relative to ωB97X-D [Chai, J.-D.; Head-Gordon, M. Phys. Chem. Chem. Phys.2008, 10, 6615], ωB97X-D3 (reoptimization of ωB97X-D with improved dispersion corrections) is shown to be superior for nonbonded interactions, and similar in performance for bonded interactions, while ωM06-D3 is shown to be superior for general applications.

15.
Mol Biol Rep ; 39(6): 6495-503, 2012 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-22314911

RESUMO

For the aging populations of any nation, Dementia is becoming a primary problem and Alzheimer's dementia (AD) is the most common type. However, until now, there is no effective treatment for AD. Tanshinone IIA (Tan IIA) has been reported for neuroprotective potential to against amyloid ß peptides (Aß)-induced cytotoxicity in the rat pheochromocytoma cell line PC-12, which is widely used as AD research model, but the mechanism still remains unclear. To investigate the effect of Tan IIA and the possible molecular mechanism in the apoptosis of PC12 cells, we induced apoptosis in PC12 cells with ß-amyloid(25-35), and treated cells with Tan IIA. After 24 h treatment, we found that Tan IIA increased the cell viability and reduced the number of apoptotic cells induced by Aß(25-35). However, neuroprotection of Tan IIA was abolished by PI3K inhibitor LY294002. Meanwhile, Treatment with lithium chloride, a phosphorylation inhibitor of GSK3ß, which is a downstream target of PI3K/Akt, can block Aß(25-35)-induced cell apoptosis in a Tan IIA-like manner. Our findings suggest that Tan IIA is an effective neuroprotective agent and a viable candidate in AD therapy and PI3K/Akt activation and GSK3ß phosphorylation are involved in the neuroprotection of Tan IIA.


Assuntos
Peptídeos beta-Amiloides/fisiologia , Apoptose/efeitos dos fármacos , Diterpenos de Abietano/farmacologia , Fármacos Neuroprotetores/farmacologia , Fragmentos de Peptídeos/fisiologia , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Animais , Proliferação de Células/efeitos dos fármacos , Ativação Enzimática , Quinase 3 da Glicogênio Sintase/genética , Quinase 3 da Glicogênio Sintase/metabolismo , Glicogênio Sintase Quinase 3 beta , Células PC12 , Fosforilação , Processamento de Proteína Pós-Traducional , Proteínas Proto-Oncogênicas c-akt/genética , Ratos , Transdução de Sinais
16.
Neural Regen Res ; 7(9): 652-8, 2012 Mar 25.
Artigo em Inglês | MEDLINE | ID: mdl-25745458

RESUMO

PC12 cell injury was induced using 20 µM amyloid ß-protein 25-35 to establish a model of Alzheimer's disease. The cells were then treated with 5, 10, and 25 µM Schisandrin B. Methylthiazolyldiphenyl-tetrazolium bromide assays and Hoechst 33342 staining results showed that with increasing Schisandrin B concentration, the survival rate of PC12 cells injured by amyloid ß-protein 25-35 gradually increased and the rate of apoptosis gradually decreased. Reverse transcription-PCR, immunocytochemical staining and western blot results showed that with increasing Schisandrin B concentration, the mRNA and protein expression of vacuolar protein sorting 35 and amyloid precursor protein were gradually decreased. Vacuolar protein sorting 35 and amyloid precursor protein showed a consistent trend for change. These findings suggest that 5, 10, and 25 µM Schisandrin B antagonizes the cellular injury induced by amyloid ß-protein 25-35 in a dose-dependent manner. This may be caused by decreasing the expression of vacuolar protein sorting 35 and amyloid precursor protein.

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