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Objective To investigate the neuroprotective effect and possible mechanism of Compound Porcine Cerebroside and Ganglio-side Injection (CPCGI) on cerebral ischemia-reperfusion injury in rats. Methods Healthy adult male Sprague-Dawley rats were divided into sham group (n=10), model group (n=10), CPCGI low dosage group (n=10) and high dosage group (n=10), and control group (Ginkgo biloba extract, n=10). All the rats was subjected to middle cerebral artery occlusion (MCAO) for two hours and reperfusion except sham group, and received treatment for fourteen days once reperfusion started. They were tested with modified Neurological Severity Score one, three, seven and fourteen days after MCAO, and adhesive-removal test and beam-walking test fourteen days after MCAO. The expression of Beclin1, PINK1 and Parkin were detected with Western blotting. Results Compared with the model group, the Neurological Severity Score reduced (P<0.05) and the time crossing the beam reduced (P<0.01) in all the medical groups fourteen days after MCAO, and the time removing the adhesive paper reduced in the CPCGI groups (P<0.01). The expression of Beclin1 and Parkin decreased and the PINK1 level increased in the model group (P<0.01), and it was reversed in all the CPCGI groups (P<0.05). Conclusion CPCGI could relieve the cerebral ischemia-re-perfusion injury in rats through the regulation in mitophagy.
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Objective To evaluate the effects of Guhong Injection on motor dysfunction in rats after cerebral ischemia-reperfusion. Methods The middle cerebral arteries were occluded for 2 hours and re-perfused in Sprague-Dawley rats. They were divided in sham group, model group, Aceglutamide group, Safflowere group and Guhong group, which were intravenously administrated with normal saline, Ace-glutamide, Safflower or Guhong 24 hours after operation, and continued for 14 days. They were tested with the beam-walking test after treat-ment. Tyrosine hydroxylase (TH) immunohistochemical staining was used to investigate the viability of neurons in the substantia nigra. Re-sults The model group spent more time in the beam-walking test than that in the sham group (P<0.01), and it decreased in the Safflower group and Guhong group compared with that in the model group (P<0.05). The TH-positive neurons decreased in the model rat compared with that in the sham group (P<0.001), and increased in both Safflower and Guhong groups compared with that in the model group (P<0.01). Conclusion Guhong administration could significantly improve the motor dysfunction in rats after cerebral ischemia-reperfusion, which might be related to provent the neurons from injury in the substantia nigra.
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Objective To study the effects of Guhong injection on the expression of vascular endothelial growth factor (VEGF) in the cortex 14 days after cerebral ischemia-reperfusion. Methods 30 male Sprague-Dawley rats were divided into sham group (n=6), ischemia group (n=6), aceglutamide injection group (n=6), Honghua injection group (n=6) and Guhong injection group (n=6). The middle cerebral ar-teries of all the rats were occluded for 2 hours and reperfusion, except the sham group. Drugs were administered once a day 24 hours after re-perfusion. The expression of VEGF in cortex was detected with enzyme-linked immunosorbent assay (ELISA) 14 days after reperfusion. Re-sults The expression of VEGF decreased in the ischemia group compared with the sham group (P<0.001), and it increased both in the ace-glutamide and Guhong injection groups compared with the ischemia group (P<0.05). Conclusion Guhong injection can significantly in-crease the expression of VEGF in the cortex 14 days after ischemia-reperfusion, which may be one of the ways for neuro-protection.
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@# Objective To evaluate the effects of Guhong Injection on motor dysfunction in rats after cerebral ischemia- reperfusion. Methods The middle cerebral arteries were occluded for 2 hours and re-perfused in Sprague-Dawley rats. They were divided in sham group, model group, Aceglutamide group, Safflowere group and Guhong group, which were intravenously administrated with normal saline, Aceglutamide, Safflower or Guhong 24 hours after operation, and continued for 14 days. They were tested with the beam-walking test after treatment. Tyrosine hydroxylase (TH) immunohistochemical staining was used to investigate the viability of neurons in the substantia nigra. Results The model group spent more time in the beam-walking test than that in the sham group (P<0.01), and it decreased in the Safflower group and Guhong group compared with that in the model group (P<0.05). The TH-positive neurons decreased in the model rat compared with that in the sham group (P<0.001), and increased in both Safflower and Guhong groups compared with that in the model group (P<0.01). Conclusion Guhong administration could significantly improve the motor dysfunction in rats after cerebral ischemia- reperfusion, which might be related to provent the neurons from injury in the substantia nigra.
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Objective To explore the effect of α-zearalanol (α-ZAL) onβ-amyloid (Aβ) induced mice and the mechanism. Methods The model was induced by intracerebroventricular injection of Aβ25-35. The mice were divided randomly into sham group, model group, estradiol benzoate (EB) group (Aβ+EB) as a positive control andα-ZAL (Aβ+α-ZAL) group. Morris water maze was used to evaluate the learning and memory ability. The levels of antioxidant enzymes and nitric oxide system in the brain tissue were detected with spectrophotometric and sotopic method. Results The escape latency was longer in the model group than in the control group (P0.05). There was no significant difference between EB group andα-ZAL group (P>0.05). Conclusionα-ZAL could improve the cognitive behavior in Aβ25-35 induced mice by increasing the antioxidant activities and de-creasing the lipid peroxidation.
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There are a large amount of neural stem cells in the olfactory system which have an active proliferation, ongoing and direc-tional differentiation and migration in order to adapt to the changing environment. The clinical findings showed that the early stages of some neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease all presented dysosmia. In recent years, the relationship be-tween air pollution and dysosmia attracts public concerns. This article introduced some research progresses in this field.
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@#Objective To explore the effect of α-zearalanol (α-ZAL) on β-amyloid (Aβ) induced mice and the mechanism. Methods The model was induced by intracerebroventricular injection of Aβ25-35. The mice were divided randomly into sham group, model group, estradiol benzoate (EB) group (Aβ+EB) as a positive control and α-ZAL (Aβ+α-ZAL) group. Morris water maze was used to evaluate the learning and memory ability. The levels of antioxidant enzymes and nitric oxide system in the brain tissue were detected with spectrophotometric and sotopic method. Results The escape latency was longer in the model group than in the control group (P<0.01), and was shorter in the EB group and α-ZAL group than in the model group (P<0.05). Compared with the control group, the level of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased, and the level of malonaldehyde (MDA), constitutive nitric oxide synthase (cNOS), inducible nitrous oxide synthesis (iNOS), and nitric oxide (NO) increased in the model group (P<0.05); compared with the model group, the level of SOD and GSH-Px increased, and the level of MDA, cNOS, iNOS and NO decreased in the EB group and α-ZAL group (P<0.05), except the level of SOD and cNOS in hippocampus in α-ZAL group (P>0.05). There was no significant difference between EB group and α-ZAL group (P>0.05). Conclusion α-ZAL could improve the cognitive behavior in Aβ25- 35 induced mice by increasing the antioxidant activities and decreasing the lipid peroxidation.
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Traditional Chinese medicine (TCM) have unique efficacy and advantages for treating diseases of central nervous system. In recent years, some researches focused on neural stem cells and neurogenesis. The researches about TCM for influencing neural stem cells bi-ological characteristics and common neurological diseases were reviewed.
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@#Objective To investigate whether octacosanol would attenuate neurotoxicity in 1-Methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP)-treated C57BL/6N mice and its potential mechanism. Methods Behavioral tests, Nissl histochemistry and Western blot were used to investigate the effects of octacosanol in this mouse model of PD. Results Oral administration of octacosanol (100 mg/kg) significantly improved behavioral outcome in mice induced by MPTP and markedly ameliorated morphological appearances of neuronal cells in striatum. Furthermore, octacosanol blocked MPTP-induced phosphorylation of p38MAPK and JNK, but not ERK1/2. Conclusion The protective effects afforded by octacosanol might be mediated by blocking the phosphorylation of p38 MAPK and JNK on the signal transduction in vivo.
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@#Objective To assess the effects of Rehmannia and Storesin (RS) on peripheral-type benzodiazepine receptors (PBRs) in early hepatic encephalopathy (HE) rats. Methods CCl4 was used to induce the HE model. The benzodiazepine binding sites of PBRs in rats cortex were studied using the specific ligands [3] PK11195. Lactulose was used in the positive medicine group, and the treatment groups received different dosages of RS. Results The specific binding and the Bmax value of [3] PK11195 both significantly increased in the model group than in the control group (P<0.01). The specific binding decreased in the medium dosage group and the high dosage group than in the model group (P<0.05), and the Bmax value of [3] PK11195RS-H decreased in the high dosage group than in the model group (P<0.01). Conclusion Rehmannia and Storesin is effective on early HE rats by decreasing the specific binding of PBRs, which could reduce the neural injury.
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@# Objective To investigate the effects of Rehmannia and Storesin (RS) on early hepatic encephalopathy (HE) in rat model.Methods HE rat model was induced by CCl4 intragastric administration. The effects of RS on serum nitric oxide (NO) and nitric oxide synthase(NOS) as well as hippocampal tumor necrosis factor α (TNF-α) level of animals were evaluated in 3 dose groups. Lactulose was usedas the positive group. Results The serum NO and NOS as well as hippocampal TNF-α level of the model rats were significantly increasedcompared with that in control animals (P<0.01). The RS high dosage treatment could significantly decrease the levels of those indexes (P<0.01). Conclusion Rehmannia and Storesin is effective on early HE by decreasing the level of serum NO and NOS as well as hippocampalTNF-α.
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@#Objective To explore the effects of octacosanol on the behavioral impairments in rats with Parkinson's disease (PD) inducedby 6-hydroxydopamine (6-OHDA). Methods The SD rats were divided into the control group (n=15), the model group (n=15), the low dosegroup (n=12), the medium dose group (n=12) and the high dose group (n=12). 6-OHDA was stereotactically injected into the right striatumof the rats at 2 sites to produce PD models. The treatment groups received octacosanol with the dose of 17.5 mg/kg, 35 mg/kg or 70 mg/kgfor 2 weeks. They were tested with apomorphine-induced rotation test, the modified Morris Water Maze, and rotarod test. Results The contralateralrotation in 30 min and escape latency were less in the medium and high dose groups than in the model group (P<0.05); the latencyand total time in the rotarod test were significantly less in all the treatment groups than in the model group (P<0.01). Conclusion Octacosanolcan decrease the impaired behaviors of rats with PD induced by 6-OHDA.
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The early characterization of the diazepam-binding sites outside the brain led to their assignment as peripheralbenzodiazepine receptors, or PBRs, to distinguish them from the central benzodiazepine receptor.Although PBR is a widely used and accepted name in the scientific community,recent data regarding the structure and molecular function of this protein increasingly support renaming it to represent more accurately its subcellular role (or roles) and putative tissue-specific function (or functions). Translocator protein (18 ku,TSPO), is proposed as a new name, regardless of the subcellular localization of the protein. This review deals with the pharmacological, structural and molecular characterization of the PBR and its role in the neuropshcopharmacology.
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@# Adenosine is an important signaling molecule of the central nervous system (CNS). Adenosine typically released in the phosphorylated form(ATP), together with neurotransmitter, both of which are encapsulated in the synaptic vesicles. Once released into the synaptic space, adenosine molecules will bind to their three categories of receptors, namely A1 receptor (A1R), A2 receptor (A2R), A3 receptor (A3R), and therefore start G protein mediated signaling pathways, resulting in various and extensive biological effects. It has been discovered in recent years that adenosine has a certain level of anti-depression effect, although its mechanisms are yet to be elucidated. This review summarized the researches focusing on anti-depression roles of both adenosine and its receptors.
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@#ObjectiveTo explore the possible mechanisms of Wuling Jun Power by the DNA microarray technique.MethodsAn experimental depression model was established by exposing the mouse to a chronic mild stress procedure. The total RNA was extracted reverse-transcripted and hybrided to the mouse 1-2 cDNA microarray (Clontech). The difference of expression profiles between control model, Wuling Jun powder and fluoxetine-treated groups were analyzed by the Image 2-1 Software.Results130 genes were significantly altered in stress group compared with the control groups. Among them, 116 genes were up-regulated and 14 genes were down-regulated. Meanwhile, 85 genes significantly changed in the Wuling Jun powder treated group with 34 genes up-regulated and 51 genes down-regulated compared with the model groups. For the Fluoxetine-treated group, 133 genes significantly changed with 35 genes up-regulated and 98 genes down-regulated compared with the model groups. These genes were associated with many aspects of life including receptor activity, protein kinases, inflammatory factors, transferrin, neurogenesis and so on.ConclusionMultiple genes were affected by the stress exposure. Altered changes of some genes were normalized by Wuling Jun powder and Fluoxetine treatment. In general, the mechanisms of Wuling Jun powder and Fluoxetine are similar, but also with minor difference.
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@# ObjectiveTo observe the imitation of menopause and the change of spatial cognition in mice administrated with D-galactose and to evaluate the molecular mechanism of estrogen to protect the function of hippocampal neurons.MethodsAdult female C57BL/6 mice were bilateral ovariectomy (OVX) and subcutaneously treated with D-galactose (100 mg/kg). In estrogen replacement therapy(ERT) mice were i.p. administrated with E2 (50 μg/kg). It took 8 weeks to induce the model and treat with ERT. Morris water maze was used test the function of spatial learning and memory. Estrogen and oxidative stress enzymes were detected by kit. 8-oxo-dG was immunohistochemical stained, and the expression of MTH1 in brain hippocampus was detected by Western blotting.ResultsThe level of E2 in blood in model group was one fifth of that in Sham group(P<0-01), and E2 level obviously increased in ERT group; the escape latency significantly prolonged in model group(P<0-01), and obviously shortened in ERT group(P<0-05). SOD and GSH-Px significantly reduced and MDA obviously increased in model group(P<0-05); and approached normal in ERT group. 8-oxo-dG as a DNA oxidative damage marker was obviously increased in the hippocampus of model group. However, the expression of DNA repair protein MTH1 significantly reduced(P<0-05), and both of them returned to normal in ERT group(P<0-05).ConclusionEstrogen can improve the function of spatial cognition in aging mice model by repairing the DNA damage of hippocampal neurons.
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@#ObjectiveTo evaluate the neurobiological characteristics of human histio-amniotic mesenchymal (hAMCs) and effect of hAMCs transplantation into the brain to treat Parkinson's disease(PD) modle mice.MethodsThe expressions of mesenchymal stem cells, neural stem cells, dopaminergic neurons and markers related to neurogenesis such as Vimentin, STRO-1, nestin, CD133, β-tubulin, TH, DAT, Ngn2 and mash-1 in hAMCs were evaluated through immunocytochemical stain; and the mRNA transcriptions of neural stem cell markers, Vimentin and nestin in hAMCs were detected by RT-PCR. The PD model was induced by MPTP(i.p.) in C57BL/6 mice transplanted with hAMCs into the right striatum. The therapeutical effect of hAMCs on PD mice was evaluated by spontaneous movement, rotating bar test and the immunohistochemistry of anti-human chondrosome and TH antibodies in striatum.ResultshAMCs induced by nerve cells culture medium, expressed mesenchymal stem cells, neural stem cells, dopaminergic neurons and other specific markers related to neurogenesis mentioned above. The frequency of spontaneous movement in PD mice was significantly increased(P<0-05), and the time of rotating bar was obviously prolonged(P<0-05) after transplantation with hAMCs.ConclusionhAMCs possess the characteristics of nerve cells after cultured in vitro and can significantly recover the damage of motor function induced by MPTP after transplantation into striatum in PD model mice.
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@#ObjectiveTo explore the effects of the conjugate prepared from the cholera toxin B subunit(CB) and nerve growth factor(NGF) on the spatial learning and memory abilities and cholinergic function.MethodsThe conjugate of CB-NGF was prepared by the improved sodium metaperiodate method and nasally administrated to the β-amyloid protein(Aβ25-35) induced amnesic mice for 7 days with 2 dosage (7-5 μg/d、15 μg/d). Spatial learning and memory abilities were evaluated by Morris water maze and cholinergic function was assessed with the choline acetyl transferase (ChAT) immunohistochemical methods.ResultsMorris water maze test showed that the escape latency in Aβ25-35-treated mice prolonged and the staying time reduced in the crossed first quadrant where the platform had been located, compared with the control mice (P<0-01). In addition, the number of ChAT positive neuron declined in the model mice(P<0-001). CB-NGF nasal administration significantly shortened the escape latency and elevated the staying time and number of ChAT positive neuron(P<0-01).ConclusionCB-NGF treatment can improve the spatial and memory performance which may involve the neuroprotection to cholinergic system.
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@#ObjectiveTo assess the effects of crude extract of Cape Jasmine in the experimental Alzheimer's model induced by Aβ25-35 and the memory acquisition impaied model induced by ibotenic acid(IBO).MethodsAlzheimer's dementia of mice was induced by Aβ25-35 i.cv. treatment and the impaired memory acquisition model was induced by IBO injected into the forebrain nucleus basalis. The effects of crude extract of Cape Jasmine on the learning and memory function of model animals were evaluated with Morris water maze and step-through test in 3 dose groups(12-5, 25, 50 mg/kg). Donepezil(0-75 mg/kg)was used in the positive control group.ResultsMorris water maze test showed that the spatial learning and memory ability of the model mice significantly improved in three crude extract of Cape Jasmine groups(P<0-05). Meanwhile, the impaired function of the rats induced by IBO significantly improved in the medium dose group(P<0-01). The electric shock latent period in step-through box test prolonged and the frequency of electric shock decreased within 3 minutes in three groups.ConclusionCrude extract of Cape Jasmine can improve the learning and memory function of mice or rat in the model group.
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@#ObjectiveTo evaluate the quantitative and qualitative changes of peripheral-type benzodiazepine recepors (PBRs) in brain mitochodria and in platelet membrane in aging rats. MethodsMale Sprague-Dawley rats were divided into 3- and 24-month groups. All animals were sacrificed by decapitation and the brains were immediately removed. Mitochondrial components from dissected cerebral cortex were isolated. The membrane of platelets from venous blood was prepared by the method of hypotonic hemolysis. The specific binding assay of the radioactive PBRs antagonist ［3H］PK11195 to membrane was performed. Scatchard analysis was performed to estimate the equilibrium dissociation constant (Kd) and the maximal binding site density (Bmax). ResultsA significant increase in ［3H］PK11195 binding activity in the mitochodria from cerebral cortex in 24-month rats was observed compared to that in 3-month rats(P<0-001). Meanwhile, the Scatchard analysis revealed that there was an increase in Bmax, with a significant increase in Kd in 24-month rats. The same change of ［3H］PK11195 binding activity was noted for platelet membrane in 24-month rats(P<0-001).ConclusionThe density of PBRs increases in cortex mitochondria in aging rats, but the binding affinity of PBRs decreases which may be attributable to the progressive pathogenesis of aging in rats. ［3H］ PK11195 binding activity of platelet membrane might reflect the change of PBRs in the brain tissue.