Mei Gao

Shenyang Pharmaceutical University, Feng-t’ien, Liaoning, China

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Publications (18)30.19 Total impact

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    ABSTRACT: Abstract Objective: To investigate whether Ginkgo biloba extract retards selenite-induced cataractogenesis in Wistar rat pups. Methods: On postpartum day eight, Group I rat pups (n = 12) received an intraperitoneal injection of physiological saline. Groups II and III rat pups (n = 12) received a subcutaneous injection of sodium selenite. Group III also received an intraperitoneal injection of G. biloba extract once daily on postpartum days 9-14. Both eyes of each pup were examined from postpartum day 16 up to day 30. After sacrifice, encapsulated pup lens were analyzed for mean activities of catalase, superoxide dismutase, glutathione peroxidase (GPx), glutathione S-transferase and glutathione reductase. In addition, the mean concentrations of reduced glutathione (GSH) and malondialdehyde were analyzed in samples of lens and serum. Results: Dense lenticular opacification occurs 100% in Group II, but only minimal opacification occurs in three pups of Group III (25%), no opacification in 75% of Group III, none in Group I. Compared with Groups I and III, Group II rat showed lower lenticular antioxidant enzyme activity, lower level of GSH, and higher level of malondidehyde (mean ± standard deviation SD, p < 0.05 respectively). Conclusions: The treatment with G. biloba extract is effective against oxidative stress - a crucial factor of cataractogenesis in rat pups, possibly by preventing depletion of antioxidant enzymes and by inhibiting lipid peroxidation.
    Current eye research. 11/2014;
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    ABSTRACT: The aim of the present study was to investigate the effect of pinocembrin on cognitive ability impairment in a rat model of transient global cerebral ischemia (TGCI). The TGCI model was established by inducing global cerebral ischemia for 20 min, followed by reperfusion for two weeks. The rats were divided into five experimental groups, including the sham group that were not subjected to ischemia, and four ischemic groups where the rats were exposed to TGCI. The sham and control TGCI groups were administered a vehicle intravenously immediately after reperfusion, while the other three groups were intravenously treated with 1, 5 and 10 mg/kg pinocembrin, respectively. In the present study, neurological scores were analyzed at 0 and 24 h after reperfusion, and the effect of pinocembrin on cognitive ability impairment in the TGCI rat model was investigated using a Morris water maze test. Neuronal loss was observed under an optical microscope with the assistance of Nissl staining. In addition, glial fibrillary acidic protein (GFAP)-positive cells were observed under an optical microscope by an immunohistochemistry assay. Pinocembrin treatment was found to alleviate the cognitive impairments, decrease the neurological scores, diminish neuronal loss in the hippocampus and reduce the number of GFAP-positive cells in the hippocampal CA1 region of the TGCI rats. Therefore, pinocembrin alleviated memory impairment in the TGCI rats.
    Experimental and therapeutic medicine 10/2014; 8(4):1285-1290. · 0.34 Impact Factor
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    ABSTRACT: Embolism is responsible for at least 20% of all stroke and half of cerebral infarctions. A number of animal models have been developed to mimic thromboembolic stroke. However, little aimed directly at hippocampal damage and cognitive function. In the present study, three sizes of emboli (150-178 μm, 74-124 μm, and 48-74 μm) were employed to induce thromboembolic stroke model in rats. Results showed that the diameter of the particle was critical for animal behavioral and histopathological consequences. Hematoxylin-eosin (HE) staining revealed that CA1 and CA2-3, which are two of the main hippocampal subdivisions were injured seriously, especially induced by emboli(48-74 μm) . At 24 hr, the neurological deficit scores showed that emboli injection could cause significant neurological deficit, and the increase of neurological deficit scores correlated well to the diameter of emboli. At 60 days, emboli(150-178 μm) and emboli(48-74 μm) lead to obvious cognitive impairment, which correlated well to the hippocampal CA1 injury. Our research might be helpful to choose suitable size of emboli to induce animal model to research subcortical ischemia and vascular dementia. However, cognitive alterations and cerebral injury following different sizes of emboli injection in rats remains a topic for future investigation. Anat Rec, 2013. © 2013 Wiley Periodicals, Inc.
    The Anatomical Record Advances in Integrative Anatomy and Evolutionary Biology 06/2013; · 1.34 Impact Factor
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    ABSTRACT: Endoplasmic reticulum stress (ER stress) is known to play a vital role in mediating ischemic reperfusion damage in brain. Our previous studies showed that pinocembrin alleviated cerebral ischemic injury in ischemia/reperfusion and vascular dementia animal models, but whether attenuation of ER stress-induced apoptosis contributes to the mechanisms remains to be elucidated. In this study, an attempt was therefore made to investigate the modulation effect of pinocembrin on ischemia/reperfusion-induced ER stress in brain. Focal cerebral ischemia/reperfusion rats were induced by middle cerebral artery occlusion (MCAO) for 2h followed by 6h reperfusion. Pinocembrin was administered in different doses (1mg/kg, 3mg/kg, and 10mg/kg, respectively) at the same time of onset of reperfusion. Neurological function and brain infarction were evaluated. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method, and flow cytometer (FCM) were used to investigate cell apoptosis in penumbra cortex. DNA fragmentation assay was also performed using electrophoresis. The expression of ER stress proteins of GRP78, CHOP/GADD153, ATF4, eIF2α phosphorylation was detected by western blot, and caspase-12 was evaluated by immunohistochemical analysis. Our results demonstrate that pinocembrin-treatment (3mg/kg and 10mg/kg) significantly reduced neurological deficit scores, infarct volume, and neuron apoptosis in the ischemia/reperfusion rats. It can also significantly modulate the protein levels by increasing GRP78 (10mg/kg) and attenuating CHOP/GADD153 expression along with caspase-12 activation (3mg/kg and 10mg/kg). At the same time, eIF2α phosphorylation was restrained and the expression of ATF4 was reduced (3mg/kg and 10mg/kg). These results suggest that the attenuation of ER stress induced apoptosis may be involved in the mechanisms of pinocembrin.
    Neuroscience Letters 05/2013; · 2.03 Impact Factor
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    ABSTRACT: AIM: To investigate the relationship between cerebroprotection of pinocembrin and epoxyeicosatrienoic acids (EETs) and their regulating enzyme soluble epoxide hydrolase (sEH). METHODS: Rats underwent middle cerebral artery occlusion (MCAO) to mimic permanent focal ischemia, and pinocembrin was administrated via tail vein injection at 10 min, 4 h, 8 h and 23 h after MCAO. After 24 MCAO, rats were re-anesthetized, and the blood and brain were harvested and analyzed. RESULTS: Pinocembrin displayed significant protective effects on MCAO rats indicated by reduced neurological deficits and infarct volume. Importantly, co-administration of 0.2 mg·kg(-1) 14, 15-EEZE, a putative selective EET antagonist, weakened the beneficial effects of pinocembrin. 14, 15-EET levels in the blood and brain of rats after 24 h MCAO were elevated in the presence of pinocembrin. In an assay for hydrolase activity, pinocembrin significantly lowered brain sEH activity of MCAO rats and inhibited recombinant human sEH activity in a concentration-dependent manner (IC50, 2.58 μmol·L(-1)). In addition, Western blot and immunohistochemistry analysis showed that pinocembrin at doses of 10 mg·kg(-1) and 30 mg·kg(-1) significantly down-regulated sEH protein in rat brain, especially the hippocampus CA1 region of MCAO rats. CONCLUSION: Inhibiting sEH and then increasing the potency of EETs may be one of the mechanisms through which pinocembrin provides cerebral protection.
    Chinese journal of natural medicines. 05/2013; 11(3):207-213.
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    ABSTRACT: Salvianolic acid A (Sal A) is a polyphenol extracted from the root of the Salvia miltiorrhiza bunge. Hydrogen peroxide (H(2)O(2)) is a major reactive oxygen species (ROS), which has been implicated in stroke and other neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. In this study, we investigated the neuroprotective effects of Sal A in human SH-SY5Y neuroblastoma cells against H(2)O(2)-induced injury. Our results showed that cells pretreated with Sal A exhibited enhanced neuronal survival and that this protection was associated with an increase in adenosine triphosphate (ATP) and the stabilization of mitochondrial membrane potential. In addition, Sal A markedly decreased the excessive activation AMP-activated protein kinase (AMPK) and the serine-threonine protein kinase, Akt, in SH-SY5Ycells induced by H(2)O(2). In conclusion, our results demonstrated that Sal A protects SH-SY5Y cells against H(2)O(2)-induced oxidative stress and these protective effects are related to stress tolerance and not energy depletion via inhibition of the AMPK and Akt signaling pathway.
    Biochemical and Biophysical Research Communications 04/2012; 421(3):479-83. · 2.28 Impact Factor
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    ABSTRACT: There are growing evidences that pinocembrin has better neuroprotective effect. In the present study, the effect of pinocembrin on mitochondrial respiratory function was evaluated in global brain ischemia/ reperfusion (4-vessel occlusion, 4-VO) rats. The results showed that pinocembrin improved the respiratory activity of 4-VO brain mitochondria, through increasing ADP/O, state 3 respiration state (V3), respiration control rate index (RCI) and oxidative phosphorylation rate (OPR). And then, the effect of pinocembrin on brain mitochondria was verified in vitro. The results showed that pinocembrin increased ADP/O, state 3 respiration state, respiration control rate index, oxidative phosphorylation rate in NADH/FADH2 dependent respiratory chain and decreased state 4 respiration state (V4) in NADH dependent respiratory chain. Pinocembrin improved ATP content in brain mitochondria in vitro and in SH-SY5Y cells.
    Yao xue xue bao = Acta pharmaceutica Sinica 06/2011; 46(6):642-9.
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    ABSTRACT: Blood-brain barrier (BBB) disruption is a major consequence of cerebral ischemia/reperfusion. Several studies have reported the neuroprotection of pinocembrin on cerebral ischemia in vivo and in vitro, but the effects of pinocembrin on BBB and its underlying mechanisms are not clear. In this study, we investigated the effects of pinocembrin on BBB functions in the global cerebral ischemia/reperfusion (GCI/R) model in rats. Neurological scores and brain edema were evaluated. BBB permeability was assessed by detecting the concentrations of Evan's blue (EB) and fluorescein sodium (NaF) in brain tissue. The pathological changes of BBB ultrastructure were observed by transmission electron microscopy. Cerebral blood flow (CBF) was measured by laser Doppler flowmetry. The effects of pinocembrin on primary cultured rat cerebral microvascular endothelial cells (RCMECs) against oxygen-glucose deprivation/reoxygenation (OGD/R) were also investigated. The results showed pinocembrin decreased neurological score and lessened brain edema induced by GCI/R. Pinocembrin also reduced the concentrations of EB and NaF in brain tissue of the GCI/R rats. And pinocembrin alleviated the ultrastructural changes of cerebral microvessels, astrocyte end-feet and neurons, and improved CBF in the GCI/R rats. In addition, pinocembrin increased the viability and mitochondrial membrane potential of cultured RCMECs induced by OGD/R. In conclusion, these data demonstrate that pinocembrin alleviates blood-brain barrier injury induced by GCI/R in rats.
    Brain research 03/2011; 1391:93-101. · 2.46 Impact Factor
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    ABSTRACT: The therapeutic effect of pinocembrin, together with the therapeutic time window, in the transient global cerebral ischemia/reperfusion (I/R) rats was investigated. Adult male Sprague-Dawley rats were subjected to global cerebral ischemia for 20 min by four-vessel occlusion. Pinocembrin (1 and 5mg/kg) was administrated intravenously 30 min before ischemia and 30 min, 2h, 6h after reperfusion, respectively. Neurological scores, brain edema and histological examination by Nissl staining were employed to assess the neuronal injury after ischemia and the neuroprotection by pinocembrin. The activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and the content of malondialdehyde (MDA) in brain tissue were tested by colorimetric assays. Alterations of neurotransmitters were determined by a high performance liquid chromatography-electrochemical method. Pinocembrin significantly ameliorated neurological deficits and brain edema, and alleviated the degree of hippocampal neuronal loss at 24h after global cerebral I/R with a broad therapeutic time window. It was found that treatment with pinocembrin reduced the compensatory increase of SOD activity and decreased the MDA level and MPO activity in a dose-dependent manner. The metabolic balance between excitatory and inhibitory amino acids was modulated by pinocembrin treatment. These findings suggest that pinocembrin provides neuroprotection against global cerebral ischemic injury with a wide therapeutic time window, which may be attributed to its antioxidative, antiinflammatory and antiexcitotoxic effects.
    Life sciences 01/2011; 88(11-12):521-8. · 2.56 Impact Factor
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    ABSTRACT: The purpose of the present study was to examine the protective action and mechanisms of pinocembrin (1) on the neurovascular unit (NVU) in permanent cerebral ischemic rats. Focal cerebral ischemia was induced by occlusion of middle cerebral artery (MCAO) in rats. Compound 1 (3, 10, or 30 mg/kg) was intravenously injected at 0, 8, 16 h after MCAO. At 24 h of occlusion, 1 alleviated neuronal apoptosis, edema of astrocytic end-feet, and the deformation of endothelial cells and capillaries as revealed by the transmission electron microscopy study. To understand the mechanisms of action, the anti-inflammation effect of 1 was examined. Compound 1 reduced the expressions of tumor necrosis factor-alpha, interleukin-1beta, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, inducible NO synthase and aquaporin-4; inhibited the activation of microglias and astrocytes; and downregulated the expression of matrix metalloproteinases (MMPs) in the ischemic brain. The ischemia-induced decreases in mRNA expressions of tight junction constituent proteins, occludin and ZO-1, were also inhibited by 1. These results indicated that 1 can protect the rat brain against ischemia injury by inhibiting the inflammatory cascade, reducing the expression of MMP-9, and preventing the integrity of tight junction. This resulted in the protective action of 1 on the NVU.
    Journal of Asian natural products research 05/2010; 12(5):407-18. · 0.61 Impact Factor
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    ABSTRACT: Salidroside is a major constituent of Rhodiola rosea L. that elicits beneficial effects for ischemic cardiovascular diseases. The aim of this study was to investigate the protective effects of salidroside on endothelial cells apoptosis induced by the hypoxia mimicking agent, cobalt chloride. After challenge with cobalt chloride for 24 h, loss of cell viability and excessive apoptotic cell death were observed in EA.hy926 endothelial cells, and the level of intracellular reactive oxygen species (ROS) increased concentration-dependently. However, the endothelial cell apoptosis and excessive ROS generation were attenuated markedly by salidroside pretreatment. In addition, salidroside inhibited activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase (PARP) induced by cobalt chloride, decreased expression of Bax and rescued the balance of pro- and anti-apoptotic proteins. These findings suggest that salidroside protects endothelial cells from cobalt chloride-induced apoptosis as an antioxidant and by regulating Bcl-2 family. Salidroside may represent a novel therapeutic agent for the treatment and prevention of hypoxia and oxidative stress-related diseases.
    Biological & Pharmaceutical Bulletin 09/2009; 32(8):1359-63. · 1.85 Impact Factor
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    ABSTRACT: Luteolin (3′,4′,5,7-tetrahydroxyflavone) is an important member of the flavonoid family. It exhibits strongly anti-inflammatory, antioxidant and phytoestrogen-like activities. In the present study, we examined the anti-amnesic and protective effects of luteolin against Aβ25-35-induced toxicity in mice. Mice were given an i.c.v. injection of aggregated Aβ25-35 peptide. The learning and memory impairments, ultrastructural changes of cerebral cortex, cerebrovascular dysfunction and neuronal changes were detected after oral administration of luteolin continuously for 8 days. Our results demonstrate that oral administration of luteolin for 8 days for those Aβ25-35-induced amnesic mice conferred robust neurovascular protection in Aβ25-35-induced amnesia, involving the improvement of the spatial learning and memory capabilities, the modulation of microvascular function, the increase of regional cerebral blood flow values, the clearance of reactive oxygen species, the improvement of cholinergic neuronal system, and the increase of brain-derived neurotrophic factor level and its receptor tyrosine kinase B expression in cerebral cortex.
    Neuroscience 06/2009; · 3.12 Impact Factor
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    ABSTRACT: This study investigated the effects of baicalein, a natural compound isolated from the root of scutellaria, on cognitive and motor ability impaired by chronic cerebral hypoperfusion in rats, as well as its effects on brain mitochondria. Rats subjected to permanent bilateral common carotid artery occlusion experienced cognitive deficits, oxidative stress and mitochondria dysfunction, which was associated with the elevation of reactive oxygen species level, the decrease of oxidative phosphorylation parameters, the loss of mitochondrial membrane potential, the reduce in Bcl-2/Bax ratio, and the release of cytochrome c. Baicalein alleviated cognitive and motor impairments and decreased mitochondria reactive oxygen species production, in accordance with its improvements on membrane potential level, oxidative phosphorylation process, mitochondrial swelling degree, Bcl-2/Bax ratio and cytochrome c release. These data indicated that baicalein might have therapeutic potential for the treatment of dementia caused by chronic cerebral hypoperfusion, contributed to its protections on brain mitochondrial homeostasis and function.
    Brain research 11/2008; 1249:212-21. · 2.46 Impact Factor
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    ABSTRACT: Pinocembrin is one of the flavonoids at the highest concentration in propolis. In this study, we investigated the neuroprotective effect of pinocembrin on ischemia/reperfusion and ischemia/reperfusion-like insults. Protection by pinocembrin was studied at the in vivo level using a model of middle cerebral artery occlusion and reperfusion in rats. Pinocembrin was administrated at the start of reperfusion. Pinocembrin markedly increased rat viability, reduced infarct volumes and neurological deficit scores in all treatment groups. Primary cortical neuronal cultures were subjected to oxygen-glucose deprivation/reoxygenation, a model of ischemia/reperfusion-like injury, and treated with pinocembrin at the start of reoxygenation. Neuronal survival rates were increased, LDH release was decreased and both neurite length and apoptosis were alleviated when pinocembrin was present during reoxygenation, and this protection was associated with the reduction of reactive oxygen species, nitric oxide and neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS), and an increase of glutathione. Moreover, DNA laddering was decreased in treatment groups of pinocembrin. Caspase-3 protein was down-regulated and PARP degradation was alleviated after pinocembrin treatments. Our results suggest that pinocembrin may be a novel therapeutic strategy to reduce cerebral ischemia/reperfusion injury, and may act by the anti-oxidative and anti-apoptotic effects.
    Brain Research 07/2008; 1216:104-15. · 2.88 Impact Factor
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    ABSTRACT: Pinocembrin is the most abundant flavonoids in propolis, and has been proven to have antioxidant, antibacterial and anti-inflammatory property. To assess the protective effects of pinocembrin on neurons, SH-SY5Y neuronal cells were pretreated with pinocembrin for 2 h followed by co-treatment with glutamate (2 mM) for 12 h. Cell viability was determined by(3,4,5-dimethylthiazol-2-yl)-2,5-diphenylte-trazolium bromide assay, and apoptosis was confirmed by cell morphology, capillary zone electrophoresis and flow cytometry assay. Cell morphology was evaluated with Hoechst33258/PI dye. Treatment with pinocembrin (10(-5), 10(-6), 10(-7) mol/l) increased cell viability dose-dependently, inhibited LDH release and attenuated apoptosis. Intracellular free [Ca(2+)] was increased after glutamate exposure, and this increase was attenuated in cells treated with pinocembrin. bax mRNA expression increased remarkably following glutamate exposure and pinocembrin treatment manifested a reduction effect. bcl-2 mRNA expression changes were not detected in groups with or without pinocembrin. Western blotting results indicated that pinocembrin treatment reduced the expression of Bax and had no effect on Bcl-2, thus decreased the Bax-Bcl-2 ratio, which is in consistent with the gene expression result. Pinocembrin could also down-regulate the expression of p53 protein, and inhibit the release of cytochrome c from mitochondria to cytosol. Thus we conclude that pinocembrin exerts its neuroprotective effects in glutamate injury model partly by inhibiting p53 expression, thus Bax-Bcl-2 ratio, and the release of cytochrome c.
    European Journal of Pharmacology 07/2008; 591(1-3):73-9. · 2.59 Impact Factor
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    ABSTRACT: Acute vascular- and neuroprotective effects of pinocembrin (1) were evaluated in a rat model of focal cerebral ischemia. Focal cerebral ischemia was induced by the middle cerebral artery occlusion (MCAO) for 24 h. 5,7-Dihydroxyflavanone (compound 1; at 3, 10, or 30 mg/kg), intravenously injected at 0, 8, and 16 h after MCAO, reduced the cerebral infarct volumes by 47, 39, and 37%, respectively, as visualized by 2,3,5-triphenyltetrazolium chloride staining (P < 0.01). Treatment with 1 also reduced brain swelling and improved behavioral deficits significantly (P < 0.01 and 0.05, respectively). To evaluate the effect of 1 on blood-brain barrier (BBB) disruption, mixture of Evans Blue (EB) and sodium fluorescein (NF) was intravenously injected immediately after MCAO. Global NF/EB uptake and fluorescence imaging of local BBB disruption were measured. Treatment with compound 1 reduced the leakage of both dyes, manifesting a preventive action in BBB integrity. This is the first time to demonstrate that 1 has acute neurovascular protective action against permanent focal cerebral ischemia. The mechanism of neurovascular protective action of 1 is under investigation.
    Journal of Asian Natural Products Research 01/2008; 10(5-6):551-8. · 0.95 Impact Factor
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    ABSTRACT: In a previous study, the ciliary neurotrophic factor (CNTF) were demonstrated to lead to weight-loss partly by up-regulating the energy metabolism and the expression of uncoupling protein-1, mitochondrial transcription factor A and nuclear respiratory factor-1 in adipose tissues or muscle. To investigate the up-stream regulators of the expression, recombinant human CNTF (rhCNTF) (0.1, 0.3 and 0.9 mg/kg/day subcutaneously) were administered to KK-Ay mice for 30 days, resulting in reduction of perirenal fat mass, serum free fatty acids and islet triacylglycerol; furthermore, the values of oral glucose tolerance test were found improved. In brown adipose tissues, the gene expressions of peroxisome proliferator-activated receptor alpha (PPARalpha) and peroxisome proliferator-activated receptor coactivator-1 alpha (PGC-1alpha) were found to be up-regulated by rhCNTF. To the best of our knowledge, the changes of gene expression of PPARalpha and PGC-1alpha represent new insights into the mechanisms of anti-diabetes by rhCNTF. In addition, the activity of mitochondrial complexII was found to be increased by rhCNTF. Stimulation of PPARalpha, PGC-1alpha, uncoupling protein-1 and enhanced activity of mitochondrial complex II may be associated with the effects of anti-diabetes. The present study indicates new mechanisms of the activity and mechanisms on anti-diabetes of rhCNTF, which may be a novel anti-diabetes reagent partly acting by enhancing energy metabolism.
    Basic &amp Clinical Pharmacology &amp Toxicology 09/2007; 101(2):78-84. · 2.12 Impact Factor
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    ABSTRACT: Ciliary neurotrophic factor (CNTF) can lead to weight loss by up-regulating energy metabolism and the expression of UCP-1 in mitochondria. To investigate the up-stream regulators of the expression of UCP-1, recombinant human CNTF (rhCNTF) (0.1, 0.3, 0.9 mg/kg/day s.c.) administered to KK-Ay mice for 30 days resulting in reductions in body weight and perirenal fat mass. In brown adipose tissues, the gene expressions of nuclear respiratory factor (NRF)-1, mitochondrial transcription factor A (TFam) and uncoupling protein (UCP)-1 were found up-regulated by rhCNTF. To the best of our knowledge, these effects represent new insights on the mechanisms of action of weight loss by rhCNTF. In addition, we also found that rhCNTF increased the activity of mitochondrial complex IV. The stimulation of NRF-1, TFam, UCP-1 and the enhanced activity of mitochondrial complex IV may be associated with remedying obesity. The result indicates that rhCNTF can enhance the expressions of NRF-1 and TFam, both of which can up-regulate the expression of UCP-1.
    European Journal of Pharmacology 06/2007; 563(1-3):77-82. · 2.59 Impact Factor

Publication Stats

222 Citations
30.19 Total Impact Points

Institutions

  • 2013
    • Shenyang Pharmaceutical University
      • School of Life Science and Biopharmaceutics
      Feng-t’ien, Liaoning, China
  • 2010
    • Peking Union Medical College Hospital
      Peping, Beijing, China
  • 2008
    • Chinese Academy of Medical Sciences
      Peping, Beijing, China
  • 2007
    • China Pharmaceutical University
      • Department of Pharmacology
      Nanjing, Jiangxi Sheng, China