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Zheng J.-M.,Fujian Medical University | Zheng J.-M.,Mindong Hospital of Ningde City | Chen X.-C.,Fujian Medical University | Lin M.,Fujian Institute of Geriatrics | And 4 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.


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.


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.


Shi Y.-Q.,Fujian Institute of Geriatrics | Huang T.-W.,Fujian Institute of Geriatrics | Huang T.-W.,Fujian Medical University | Chen L.-M.,Fujian Institute of Geriatrics | And 7 more authors.
Journal of Alzheimer's Disease | Year: 2010

It is well established that the presence of soluble amyloid-β protein (Aβ) correlates with the severity of dementia in Alzheimer's disease (AD). Several lines of evidence indicate that cyclic AMP responsive element binding protein (CREB) and protein kinase A (PKA) are involved in soluble Aβ-trigged disruption of synaptic plasticity in early AD. Previously we demonstrated the beneficial effects of ginsenoside Rg1 on Aβ-induced neuronal insult. Therefore, in the present study, we examined the effects of long-term consumption of Rg1 on the cerebral Aβ content and PKA/CREB signaling molecules, as well as cognitive performance in senescence-accelerated mouse prone 8 (SAMP8). Notably, a significant dose-dependent reduction of soluble Aβ 1-40 was shown in the hippocampus of SAMP8 mice after administration with ginsenoside Rg1 for 3 months. Furthermore, Rg1 treatment resulted in a significant decrease of hippocampal PKA RIIα level (isoform IIα of the regulatory subunit of PKA). In contrast, phospho-CREB and brain derived neurotrophic factor (BDNF) levels were dramatically increased in the hippocampus of SAMP8 treated with Rg1. Additionally, administration of ginsenoside Rg1 consequently improved learning and memory outcomes in SAMP8 mice. These data suggest that long-term consumption of ginsenoside Rg1 may delay cognitive decline, associated with significant effects on Aβ generation, PKA/CREB activity, as well as BDNF content in the brain. These data provide further support for the therapeutic or intervention potency of ginsenoside Rg1 in the early stage of AD. © 2010 - IOS Press and the authors. All rights reserved.


PubMed | Fujian Institute of Geriatrics
Type: Journal Article | Journal: Journal of Alzheimer's disease : JAD | Year: 2010

It is well established that the presence of soluble amyloid-beta protein (Abeta) correlates with the severity of dementia in Alzheimers disease (AD). Several lines of evidence indicate that cyclic AMP responsive element binding protein (CREB) and protein kinase A (PKA) are involved in soluble Abeta-trigged disruption of synaptic plasticity in early AD. Previously we demonstrated the beneficial effects of ginsenoside Rg1 on Abeta-induced neuronal insult. Therefore, in the present study, we examined the effects of long-term consumption of Rg1 on the cerebral Abeta content and PKA/CREB signaling molecules, as well as cognitive performance in senescence-accelerated mouse prone 8 (SAMP8). Notably, a significant dose-dependent reduction of soluble Abeta(1-40) was shown in the hippocampus of SAMP8 mice after administration with ginsenoside Rg1 for 3 months. Furthermore, Rg1 treatment resulted in a significant decrease of hippocampal PKA RIIalpha level (isoform IIalpha of the regulatory subunit of PKA). In contrast, phospho-CREB and brain derived neurotrophic factor (BDNF) levels were dramatically increased in the hippocampus of SAMP8 treated with Rg1. Additionally, administration of ginsenoside Rg1 consequently improved learning and memory outcomes in SAMP8 mice. These data suggest that long-term consumption of ginsenoside Rg1 may delay cognitive decline, associated with significant effects on Abeta generation, PKA/CREB activity, as well as BDNF content in the brain. These data provide further support for the therapeutic or intervention potency of ginsenoside Rg1 in the early stage of AD.


PubMed | Email and Fujian Institute of Geriatrics
Type: Journal Article | Journal: Zhonghua yi xue za zhi | Year: 2014

To explore the effects of aging on the levels of reproduction-related mRNA genes including Gnrh, KISS1/KISS1r, estrogen receptor-alpha (ER), estrogen receptor-beta (ER) and progesterone receptor (PR) in hypothalamus.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).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 ER 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 ER 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 ER 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.Higher levels of ER 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.

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