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Objective To investigate the effects of cornel iridoid glycoside (CIG) on the learning-memory ability and pathological changes in the brain of vascular dementia (VD) rats; To discuss relevant mechanism of action. Methods SD rats were randomly divided into sham-operation group, model group, positive medicine group, CIG groups low-, medium- and high-dose groups. The animal model of VD was replicated by permanent bilateral common carotid artery occlusion (2VO) in rats. Drugs were intragastrically administered 6 h after surgery and then once a day for 3 months. Morris water maze test was used to detect spatial learning-memory ability, and recognition memory was measured by the object recognition test. Immunohistochemical staining was used to detect the neuronal survival and the expression of choline acetyltransferase (ChAT) in the brain. Results Three months after permanent 2VO operation, the model rats showed a longer escape latency in Morris water maze, a lower discrimination index in the object recognition test, and a decrease in NeuN positive neuronal survival and ChAT expression in the hippocampus and cerebral cortex. Compared with the model group, intragastric administration of CIG for 3 months shortened the escape latency in Morris water maze, elevated the discrimination index in the object recognition test, and increased the NeuN positive neuronal survival in the hippocampus and cerebral cortex and ChAT expression of 2VO rats. Conclusion CIG can improve the cognitive impairment of VD model rats through protecting neurons and promoting ChAT expression.
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OBJECTIVE: To study the protective effects of sparstolonin B(8,5'-dihydroxy-4-phenyl-5,2'-oxidoisocoumarin, SsnB) on mouse with intracerebral haemorrhage (ICH). METHODS: The effect of SsnB on neuronal cell death induced by Hb using a microglia-neuron transwell system was investigated. Autologous nonanticoagulated blood was collected from the tail artery of the mouse and then injected into the striatum using a syringe pump. Neurological deficit of the mouse with ICH was assessed 1,3,5 and 7 d after SsnB administration using modified neurological severity score system, and brain water content of the mouse cerebral tissues after ICH was measured at the same day. The concentrations of pro-inflammatory cytokines in perihematoma tissues, including interleukin-6, interleukin-1 p and tumor necrosis factor-α, were measured by ELISA assay. RESULTS: The results show that SsnB significantly reduced the neurological deficit scores and the brain water content, and inhibited the levels of IL-6, IL-1β and TNF-α at first day and third day after ICH. CONCLUSION: SsnB can improve the brain injury in mouse induced by ICH. The mechanism may involve increased the neuronal survival rate and decreased expression of pro-inflammatory cytokines of mouse after ICH.
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Neurons and glia in the central nervous system can express the key enzymes for the synthesis of neurosteroids .Once the concentration of neurosteroids is high enough , they will exert paracrine effects .Synthesis of neurosteroids declines with age in brain .So does it under stressful circumstances .Recent research reports indicate that the decrease of neurosteroids is associated with the neuronal dysfunction and degeneration in the brain .This paper reviews recent research on the most studied neurosteroids ( for example , dehydroepiandrosterone , pregnenolone and their sulphate esters, progesterone and allopregnanolone ) in affecting neuronal survival , neurite outgrowth and neurogenesis , and the potential roles of these neurosteroids in the treatment of neurodegenerative disease as well .
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Objective To observe olfactory ensheathing cells transplantation on brain injury recovery nerve function and to explore its mechanism. Methods After purification of the olfactory ensheathing cells cultured for NGFRp75 immunocytochemical identification and preparation of cell suspension for transplantation, some cells were pre-labeled for bservation of survival after transplantation. 48 adult SD rats were randomly divided into three groups:sham operation without injury group (A group),cerebral cortex motor area injury group (B group) , the same brain injury and the olfactory ensheathing cell transplantation group (C group). At postoperative day,3 d, 7 d,14 d the neurological severity score (NSS) of rats were assessed; 14 d after injury of brain tissues were taken for NeuN immunohistochemistry host the number of neurons change. The data were statistically analyzed using SPSS17.0 software. Results (1) Cultured olfactory ensheathing cells showed NCFRp75 positive,the positive rate was 90%. (2) 14 d after transplantation of nuclear fluorescence labeling of olfactory ensheathing cells survived well in the host body. (3) 14 d after NSS score of B group( 2.00 ± 0.53) and C group ( 1.25 ± 0.46) were significantly better than the B group (P<0.05). (4) NeuN positive cells in B group (39.2 ±7. 1) and C group(45, 8 ± 6.0) were significantly better than B group (P<0.05). Conclusions Olfactory ensheathing cell transplantation can promote the recovery of neurological function in rats brain injury,which may be related with olfactory ensheathing cells to promote neuron survival in the host.
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Objective To research the effects of neural stem cells (NSCs) transplantation on the neurological function improvement and neural survive and axonal regeneration in traumatic rat brain. Methods NSCs were cultured in vitro, labeled with hochest and transplanted into rat brain injured area by weight-dropping. Neurological severity scores(NSS) tested the functions at the 0,3,7,14 day post-injury. Immunofluorescence was used to detect the expressions of NeuN cells and GAP-43. Results There was significant difference in NSS between NSCs transplantion group and brain injury group(4.38 ±0.74 vs 5.50 ± 1.07, P＜0.01) at 7th day. There were a significant increase in neural number (51.46 ± 3. 303 vs 42.83 ± 5. 401, P ＜ 0.01 ) ), and GAP-positive axons ( 13.3 ± 1.7 vs 8.7 ± 1.1, P＜0.01 ) in NSCs transplantion group than in control group. Conclusion NSCs have an effects on the neurological improvement in brain injured rat. This may be associated to the increase in number of the neurons and local axons.
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@#Objective To observe the effects of cornel iridoid glycoside (CIG) on nervous function and neuronal survival in focal cerebral ischemic rat model.MethodsThe animal model was induced by occlusion of middle cerebral artery with suture embolus. Nervous function defect and survival number of neuron were detected with nervous function score and Nissl's staining respectively.ResultsCompared with Sham operation group, nervous function score increased and nervous survival number decreased obviously in model rats. Compared with model group, CIG decreased nervous function score and increased survival neurons significantly. ConclusionCIG may have theraputic effect on cerebral infarct through improving nervous function and increasing survival neurons.
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Objective Whether combination of ganoderma spore and L-NNA(NOS inhibitor) could promote the neuronal survival and axonal regeneration in Clarke's nucleus(CN) and red nucleus(RN) following spinal cord hemisection was explored. Methods Thirty adult female rats were divided into control group,L-NNA group,low dosage of ganoderma spore group,low dosage of ganoderma spore+L-NNA group,high dosage of ganoderma spore group and high dosage of ganoderma spore+L-NNA group.L-NNA was intraperitoneally injected and high dosage of ganoderma spore was irrigated into the rat's stomach after hemisection of T11 spinal cord segment in high dosage of ganoderma spore+L-NNA group. Results Thirty days after spinal cord hemisection,the number of CN neurons was decreased and some neurons were expressing NOS on lesioned side of L1 spinal cord in control group.The number of CN neurons on lesioned side of L1 spinal cord was increased in L-NNA group and low dosage of ganoderma spore group,but the number of NOS-positive neurons was decreased.In low dosage of ganoderma spore+L-NNA group and high dosage of ganoderma spore group,the number of CN neurons was significantly increased and NOS-positive neurons were also significantly decreased on lesioned side of L1 spinal cord.In high dosage of ganoderma spore+L-NNA group,there were most CN neurons surviving and least NOS-positive CN neurons,and some neurons were labeled by flourogold on lesioned side of LI spinal cord.The density of RN neurons on lesioned side was decreased in control group and L-NNA group.The density of RN neurons on lesioned side was increased in low dosage of ganoderma spore group and low dosage of ganoderma spore+L-NNA group.The density of RN neurons on lesioned side was significantly increased in high dosage of ganoderma spore group and high dosage of ganoderma spore+L-NNA group.Conclusion Ganoderma spore or L-NNA can promote the survival of injuried CN neurons after spinal cord hemisection.Combination of ganoderma spore and L-NNA can better promote injuried CN neuronal survival and axonal regeneration.Ganoderma spore can also enhance injuried RN neuronal survival.
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Objective To explore the effects of Ganoderma spore(germination activated Ganoderma spore) on survival and expression of neurotrophin_3(NT_3) and nitric oxide synthase(NOS) of injured motor neurons in rat spinal cord. Methods Different dosages of Gandoerma spore were irrigated into the rat's stomach respectively in experimental groups after oneside ventral root cut.The survival ratio of injured motor neurons was counted.NT_3 expression of surviving motor neurons was measured by immunohistochemistry and in situ hybridization methods and NOS activity was measured by enzymo_histochemistry method. Results Thirty_five days after ventral root cut,the survival ratio of motor neurons was 47.32% in control group,and those were 67.11%,72.67% and 81.67% respectively in low,medial and high dosage Ganoderma spore groups.Expressions of NT_3 and NOS of surviving motor neurons in high dosage Ganoderma spore group were higher than those in control group.Conclusion Ganoderma spore may promote the survival of injured spinal motor neurons,and survival ratio of injured motor neurons is related to the dosages of Ganoderma spore.Ganoderma spore may also enhance the expressions of NT_3 and NOS of surviving spinal motor neurons.