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Wu B.,Southern Medical University | Wu B.,Neurosurgery Institute of Beijing Military Region | Yao X.,Affiliated Bayi Brain Hospital | Yao X.,Neurosurgery Institute of Beijing Military Region | And 4 more authors.
DNA and Cell Biology | Year: 2013

DNA methylation plays an essential role in carcinogenesis. Promoter hypermethylation can result in transcriptional silencing of specific genes, such as tumor suppressors. Thus far, few reports have investigated the effect of curcumin, an active component of the perennial herb Curcuma longa, on DNA methylation. In the present study, we evaluated the effects of curcumin on receptor activator of NF-κB (RANK) gene expression in human glioblastoma cells. Incubation of cells with therapeutic concentrations of curcumin resulted in a significant elevation of RANK expression at both the mRNA and protein levels in two glioblastoma cell lines. We further confirmed that this elevation was associated with promoter demethylation through methylation-specific polymerase chain reaction (PCR) and bisulfite sequencing PCR. Additionally, we demonstrated that knockdown of STAT3, an oncogenic transcription factor, is sufficient to induce RANK promoter demethylation along with RANK reactivation. These results demonstrated that curcumin induced RANK gene reactivation through epigenetic modification in human glioblastoma cells, and that STAT3 is involved in RANK promoter hypermethylation and epigenetic silencing, thus allowing for further applications of curcumin epigenetic therapy in glioma and therapeutic implications of STAT3 in human glioblastoma. © Mary Ann Liebert, Inc. 2013. Source

Chen F.,Chongqing Medical University | Wang H.,Chongqing Medical University | Xiang X.,Chongqing Medical University | Yuan J.,Chongqing Medical University | And 7 more authors.
Journal of Surgical Research | Year: 2014

Background: The objective of the present study was to clarify the relationship between the neuroprotective effects of curcumin and the classical wnt signaling pathway. Method: Using Sprague-Dawley rats at a gestational age of 14.5 d, we isolated neural stem cells from the anterior two-thirds of the fetal rat brain. The neural stem cells were passaged three times using the half media replacement method and identified using cellular immunofluorescence. After passaging for three generations, we cultured cells in media without basic fibroblast growth factor and epidermal growth factor. Then we treated cells in five different ways, including a blank control group, a group treated with IWR1 (10 μmol/L), a group treated with curcumin (500 nmol/L), a group treated with IWR1 + curcumin, and a group treated with dimethyl sulfoxide (10 μmol/L). We then measured the protein and RNA expression levels for wnt3a and β-catenin using Western blotting and Reverse transcription-polymerase chain reaction (RT-PCR). Results: Western-blotting: after the third generation of cells had been treated for 72 h, we observed that wnt3a and β-catenin expression was significantly increased in the group receiving 500 nmol/L curcumin but not in the other groups. Furthermore, cells in the IWR1-treated group showed decreased wnt3a and β-catenin expression, and wnt3a and β-catenin was also decreased in the IWR1 + 500 nmol/L curcumin group. No obvious change was observed in the dimethyl sulfoxide group. RT-PCR: RT-PCR showed similar changes to those observed with the Western blotting experiments. Conclusions: Our study suggests that curcumin can activate the wnt signaling pathway, which provides evidence that curcumin exhibits a neuroprotective effect through the classical wnt signaling pathway. © 2014 Elsevier Inc. All rights reserved. Source

Yuan J.,Chongqing Medical University | Zou M.,Affiliated Bayi Brain Hospital | Xiang X.,Chongqing Medical University | Zhu H.,Chongqing Medical University | And 4 more authors.
Journal of Surgical Research | Year: 2015

Background Spinal cord injury (SCI) is characterized by a high rate of disability and imposes a heavy burden on society and patients. SCI can activate glial cells and lead to swelling, hyperplasty, and reactive gliosis, which can severely reduce the space for nerve growth. Glial cells can secrete a large amount of extracellular inhibitory components, thus altering the microenvironment of axon growth. Both these factors seriously impede nerve regeneration. In the present study, we investigate whether curcumin (cur), a phytochemical compound with potent anti-inflammatory effect, plays a role in the repair of SCI. Materials and methods We established a rat model of SCI and treated the animals with different concentrations of cur. Using behavioral assessment, immunohistochemistry, real-time polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay, we detected the intracellular and extracellular components of glial scar and related cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, nuclear factor (NF)-κb, transforming growth factor (TGF)-β1, TGF-β2, and sex determining region Y-box (SOX)-9. Results We found that cur inhibited the expression of proinflammatory cytokines, such as TNF-α, IL-1β, and NF-κb; reduced the expression of the intracellular components glial fibrillary acidic protein through anti-inflammation; and suppressed the reactive gliosis. Also, cur inhibited the generation of TGF-β1, TGF-β2, and SOX-9; decreased the deposition of chondroitin sulfate proteoglycan by inhibiting the transforming growth factors and transcription factor; and improved the microenvironment for nerve growth. Through the joint inhibition of the intracellular and extracellular components of glial scar, cur significantly reduced glial scar volume and improved the Basso, Beattie, and Bresnahan locomotor rating and axon growth. Conclusions Our data support a role for curcumin in promoting neural function recovery after SCI by the joint inhibition of the intracellular and extracellular components of glial scar, providing an important strategy for treating SCI. © 2015 Elsevier Inc. All rights reserved. Source

Zhang H.-T.,Affiliated Bayi Brain Hospital | Xue S.,Southern Medical University | Li P.-J.,Affiliated Bayi Brain Hospital | Fu Y.-B.,Affiliated Bayi Brain Hospital | Xu R.-X.,Affiliated Bayi Brain Hospital
Clinical Neurology and Neurosurgery | Year: 2013

Objective: There is limited information available regarding the treatment of huge hypertensive putaminal hemorrhage (HPH). This study aimed to evaluate our experience of 33 patients with huge HPH who were treated by open surgery (decompressive craniectomy and hematoma evacuation) and external cerebrospinal fluid (CSF) drainage. Methods: We reviewed the records of 33 consecutive patients admitted to our hospital with huge HPH (≥60 cm3). All patients were treated by decompressive craniectomy, hematoma evacuation, and CSF drainage. Data collected included age, gender, blood pressure at admission, Glasgow Coma Scale (GCS) score, intracranial hemorrhage (ICH) location, ICH volume, degree of midline shift, presence/absence of basal cistern obliteration at admission and before surgery, and presence/absence of intraventricular hemorrhage (IVH). Outcome was assessed by the Glasgow Outcome Scale score at 30 days after surgery. Results: The median GCS score was 5.0 at admission, and improved to 8.0 at 1 week after surgery. The median ICH volume was 95 cm 3 before surgery and 4 cm3 after surgery. IVH was observed in 93.9% of patients. The overall survival rate to discharge was 75.6% (25/33), including 15.1% (4/33) with good function, 36.4% (12/33) with disability, and 24.3% (8/33) in a vegetative state. The mortality rate was 24.3% (8/33). Patients with right-sided ICH had better outcomes than those with left-sided ICH. No patients with GCS score ≤6 and ICH volume ≥90 cm3 at admission achieved good postoperative function. Operative time was significantly shorter with hematoma evacuation via the transcortical approach than via the transsylvian approach (3.41 ± 0.75 h vs. 4.14 ± 0.59 h, P < 0.001). There were no significant differences in the rates of mortality or survival with good function between the two groups. Conclusions: Treatment of huge HPH by decompressive craniectomy, hematoma evacuation, and CSF drainage is life-saving. Patients with GCS score 7-8, ICH volume 60-90 cm3, and right-sided ICH may achieve good recovery. The transcortical approach appears to be more effective than the transsylvian approach for rapid decompression of the edematous brain. © 2013 Elsevier B.V. Source

Wu B.,Southern Medical University | Wu B.,Neurosurgery Institute of Beijing Military Region | Yao H.,Affiliated Bayi Brain Hospital | Yao H.,Neurosurgery Institute of Beijing Military Region | And 4 more authors.
Biochemical and Biophysical Research Communications | Year: 2013

Curcumin, an active polyphenol extracted from the perennial herb Curcuma longa, controls various molecules involved in tumor cell death. In this study, we found that the tumor suppressor death-associated protein kinase 1 (DAPK1) plays a vital role in the anti-carcinogenic effects of curcumin. We found that curcumin increased DAPK1 expression at the mRNA and protein levels in U251 cells, and that the siRNA-mediated knockdown of DAPK1 attenuated the curcumin-induced inhibition of STAT3 and NF-κB. Moreover, DAPK1 suppression diminished curcumin-induced caspase-3 activation. In addition, we confirmed that DAPK1 was required for a curcumin-induced G2/M cell cycle arrest and apoptosis. Thus, DAPK1 is involved in curcumin-mediated death pathways. Our data suggest novel mechanisms for curcumin in cancer therapy. © 2013 Elsevier Inc. Source

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