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Yao P.-S.,Fujian Medical University | Kang D.-Z.,Fujian Medical University | Lin R.-Y.,Fujian Medical University | Ye B.,Fujian Institute of Geriatrics | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2014

Glioma glutamate release has been shown to promote the growth of glioma cells and induce neuronal injuries from epilepsy to neuronal death. However, potential counteractions from normal astrocytes against glioma glutamate release have not been fully evaluated. In this study, we investigated the glutamate/glutamine cycling between glioma cells and astrocytes and their impact on neuronal function. Co-cultures of glioma cells with astrocytes (CGA) in direct contact were established under different mix ratio of astrocyte/glioma. Culture medium conditioned in these CGAs were sampled for HPLC measurement, for neuronal ratiometric calcium imaging, and for neuronal survival assay. We found: (1) High levels of glutaminase expression in glioma cells, but not in astrocytes, glutaminase enables glioma cells to release large amount of glutamate in the presence of glutamine. (2) Glutamate levels in CGAs were directly determined by the astrocyte/glioma ratios, indicating a balance between glioma glutamate release and astrocyte glutamate uptake. (3) Culture media from CGAs of higher glioma/astrocyte ratios induced stronger neuronal Ca 2+ response and more severe neuronal death. (4) Co-culturing with astrocytes significantly reduced the growth rate of glioma cells. These results indicate that normal astrocytes in the brain play pivotal roles in glioma growth inhibition and in reducing neuronal injuries from glioma glutamate release. However, as tumor growth, the protective role of astrocytes gradually succumb to glioma cells. © 2014 Elsevier Inc. All rights reserved.

Zhang J.,Fujian Institute of Geriatrics | Yang L.-M.,Fujian Institute of Geriatrics | Chen X.-C.,Fujian Institute of Geriatrics
National Medical Journal of China | Year: 2013

Objective: To explore the effects of aging on the levels of reproduction-related mRNA genes including Gnrh, KISS1/KISSlr, estrogen receptor-alpha (ERα), estrogen receptor-beta (ERβ) and progesterone receptor (PR) in hypothalamus. Methods: Proestrus and metestrus in young (3-4 months) and middle-aged (10-11 months) female mice and diestrus in senile (18-19 months) female mice were observed. And the levels of related mRNA genes in preoptic area anterior hypothalamus (POA-AH) and medial basal hypothalamus (MBH) were determined by real-time polymerase chain reaction (RT-PCR). Results: In middle-aged mice on proestrus, the level of Gnrh mRNA in POA-AH (0.896±0.049) was significantly lower than that in young mice (1.228±0.147, P=0.049). The level of ERα mRNA in POA-AH decreased in young mice on proestrus whereas increased in middle-aged mice (0.432±0.063 vs 0.603±0.018, P=0.016). The level of ERα mRNA of POA-AH, both in middle-aged mice (0.432±0.063, P=0.014) and senile mice (0.403±0.145, P=0. 020) on diestrus, were significantly lower than that in young mice. The PR mRNA expression in middle-aged mice on proestrus (1.037±0.037) was markedly lower than that in young mice(1.251±0.081, P=0.031). In senile mice, the levels of Gnrh mRNA (1.520±0.146, P=0.004) and ERβ mRNA (1.572±0.184, P=0.011) increased in POA-AH compared with that in young mice on metestrus. Aging had no effect upon KISS1 and KISS1r mRNA levels in POA-AH. In contrast, KISS1 mRNA level of MBH in middle-aged (1.663±0.398, P=0.037) and senile (2.622±0.454, P=0.014) mice obviously increased compared with the young mice group. Conclusion: Higher levels of ERa mRNA and decreases of PR and Gnrh mRNA in POA-AH in middle-aged mice on proestrus may play an important role in declining reproductive function. Copyright © 2013 by the Chinese Medical Association.

Zhan Z.-T.,Fujian Medical University | Ye Q.-Y.,Fujian Medical University | Zhu Y.-G.,Fujian Medical University | Zhu Y.-G.,Fujian Institute of Geriatrics | And 2 more authors.
Acta Anatomica Sinica | Year: 2010

Objective To investigate periventricular white matter change and matrix metalloproteinase-2 and 7 (MMP-2 and MMP-7) expression after chronic cerebral hypoperfusion in rats. Methods Sixty healthy male Wistar rats were randomly divided into sham-operated (control) group and three model groups(20 days, 40 days and 60 days). Model of chronic cerebral hypoperfusion was induced by staging permanent ligation of the bilateral common carotid arteries in the rat. The ultrastructure change in periventricular white matter was observed with transmission electron microscopy. The activation of astrocytes was assessed with immunohistochemistry staining of glial fibrillary acidic proteinl(GFAP), and the expressions of MMP-2, 7 and myelin basic protein(MBP) were detected with immunohisitochemisty staining and Western blotting. Results Irregular myelin sheaths and degenerating myelinated axon were observed at the ultrastructural level in the corpus callosum and internal capsule of the 20 days operated rats. Obvious proliferation hypertrophy of GFAP immunopositive astrocytes were observed and the expression of GFAP gradually increased in the model groups, while the content of MBP decreased (P < 0. 01). The expressions of MMP-2 and MMP-7 were markedly elevated in the model groups(P < 0. 01 or P < 0. 001 ). Additionally, the up-regulation of MMP-2 and MMP-7 showed a significant relation with periventricular white matter matter lesions. Conclusion Chronic cerebral hypoperfusion induces progressive periventricular white matter lesions with the up-regulation of MMP-2 and MMP-7 which may involve in the pathological process of white matter lesions.

Zheng J.-M.,Fujian Medical University | Chen X.-C.,Fujian Medical University | Lin M.,Fujian Institute of Geriatrics | Zhang J.,Fujian Institute of Geriatrics | And 3 more authors.
Yaoxue Xuebao | Year: 2011

The probable mechanism of the reduction of rat cerebral ischemic-reperfusion injury by propyl gallate was studied. Intraluminal suture middle cerebral artery occlusion model of rat was employed. Propyl gallate was injected immediately after the ischemia was happened. The activity of NF-κ, and the expression of COX-2 and HSP70 on the peripheral ischemia were determined by Western blotting. The expression of TNF-α was determined by ELISA assay. RT-PCR and immunofluorescence staining were employed to detect the transcription and expression of TLR-4. Results showed that propyl gallate could inhibit the activity of NF-κB in the peripheral ischemia, and reduce the expression of COX-2 and TNF-α. As the upstream of NF-κB, the transcription and expression of TLR-4 decreased, as well as HSP70, the endogenic ligand of TLR-4. As an antioxidant, propyl gallate could reduce the cerebral ischemic-reperfusion injury through inhibiting the activity of NF-κB and decreasing the COX-2 and TNF-α in the peripheral ischemia. It also could influence HSP70 and TLR-4.

Wu M.,Fujian Institute of Geriatrics | Wu M.,Fujian Medical University | Zhu Y.-G.,Fujian Institute of Geriatrics | Zhu Y.-G.,Fujian Medical University | And 8 more authors.
Yaoxue Xuebao | Year: 2010

This study is to explore whether the Wnt/β-catenin signaling pathway is involved in the process of tripchlorolide (T 4) protecting against oligomeric Aβ 1-42-induced neuronal apoptosis. Primary cultured cortical neurons were used for the experiments on day 6 or 7. The oligomeric Aβ 1-42 (5 μmol·L -1 for 24 h) was applied to induce neuronal apoptosis. Prior to treatment with Aβ 1-42 for 24 h, the cultured neurons were pre-incubated with T 4 (2.5, 10, and 40 nmol·L -1), Wnt3a (Wnt signaling agonists) and Dkk1 (inhibitors) for indicated time. Then the cell viability, neuronal apoptosis, and protein levels of Wnt, glycogen synthase kinase 3β (GSK3β), β-catenin and phospho-β-catenin were measured by MTT assay, TUNEL staining and Western blotting, respectively. The result demonstrated that oligomeric Aβ 1-42 induced apoptotic neuronal cell death in a time- and dose-dependent manner. Pretreatment with T 4 significantly increased the neuronal cell survival and attenuated neuronal apoptosis. Moreover, oligomeric Aβ 1-42-induced phosphorylation of β-catenin and GSK3β was markedly inhibited by T 4. Additionally, T 4 stabilized cytoplasmic β-catenin. These results indicate that tripchlorolide protects against the neurotoxicity of Aβ by regulating Wnt/β-catenin signaling pathway. This may provide insight into the clinical application of tripchlorolide to Alzheimer's disease.

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