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Objective: To investigate the effect of vitexin on oxidative stress in rats with acute cerebral ischemia-reperfusion by regulating the pathway of nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE). Methods: A total of 54 SD rats were randomly divided into Sham group, model group, positive control (edaravone 0.56 mg/kg) group and vitexin low, medium, and high dose (10, 20, 40 mg/kg) groups. The rat models with acute cerebral ischemia were established except the Sham group. After reperfusion, rats in Sham group and model group were received ip saline. The edaravone group and vitexin groups were administered according to the corresponding dose, once every 8 h for a total of three times. The neurobehavioral scores of rats before and after intervention were compared. HE staining was used to detect the pathological changes of cerebral cortex. The levels of MDA, NO, SOD, and GSH in cerebral cortex of rats were detected by the kit. The mRNA and protein expression levels of Nrf2/ARE pathway related gene in rat cerebral cortex were detected by real-time fluorescent quantitative PCR (qRT-PCR) and Western blotting. Results: Before and after intervention, there was no significant change in the neurobehavioral score of rats in the Sham group, the model group was higher than before intervention (P < 0.01), the edaravone group and the vitexin groups were lower than before intervention (P < 0.01), and there was a significant difference in the neurobehavioral score between the groups after intervention (P < 0.01). In the Sham group, the distribution of nerve cells was uniform and dense, and the morphology of cell body and nucleus was normal. In the model group, edaravone group and vitexin group, the arrangement of brain tissue was disordered and loose, in which liquefying necrosis and disappearance of cell structure were observed in the model group; in the low-dose group, the arrangement of cells was seriously disordered and loose. In the vitexin medium dose group and edaravone group, the area of liquefying necrosis was small, and most of the cells were normal; In the vitexin high dose group, only a few liquefying necrosis were found, the cell structure was basically normal, and the cell arrangement was slightly disordered. Compared with the Sham group, the levels of MDA and NO in the cerebral cortex of the model group were significantly increased (P < 0.01), the levels of SOD and GSH were significantly reduced (P < 0.01), and the expression levels of Nrf2 and γ-GCS mRNA were significantly increased (P < 0.01), the expression of cytoplasmic Nrf2 and γ-GCS proteins were significantly increased (P < 0.01), and the expression levels of nuclear Nrf2 and HO-1 proteins were significantly decreased (P < 0.01). Compared with the model group, the levels of MDA and NO in the cerebral cortex of rats in the edaravone group and low, medium and high dose groups of vitexin were significantly reduced (P < 0.01), and the levels of SOD and GSH were significantly increased (P < 0.01), Nrf2 and γ-GCS mRNA expression levels were significantly reduced (P < 0.01), cytoplasmic Nrf2, γ-GCS protein expressions were significantly reduced (P < 0.01), and nuclear Nrf2 and HO-1 protein expression levels were significantly increased (P < 0.01). And the levels of MDA, NO, SOD, GSH and Nrf2, γ-GCS, HO-1 mRNA and protein expression in rat cerebral cortex in each dose group were dose-dependent, with significant differences between groups (P < 0.01). Conclusion: Vitexin can alleviate oxidative stress in rats with acute cerebral ischemia-reperfusion. It is speculated that it is related to the regulation of Nrf2/ARE signaling pathway, the up-regulation of Nrf2 gene and protein expression, the promotion of its movement from cytoplasm to nucleus, the up-regulation of HO-1 expression, the inhibition of γ-GCS expression, and the enhancement of the body’s ability to response to oxidative stress.
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Objective: To investigate the neuroprotective effect of vitexin (VT) on acute cerebral ischemia (ACI) reperfusion rats and its effect on helper T cell 1 (Th1)/Th2 drift. Methods: Rat models of ACI reperfusion were established and divided into model group, low, medium and high doses of VT (0.94, 1.88, 3.76 mg/kg) groups and sham operated group. After 1 h of ischemia-reperfusion, rats in different doses of VT were given different concentrations of VT by ip, and rats in sham operated group and model group were given the same amount of saline by ip for three consecutive days. The general state of rats was observed. Longa neurological score before and after administration, and morphological changes of neurons in brain tissue after administration were evaluated and compared. The damage rates of single and double strands breaks of DNA in brain tissue were compared. The levels of Th1 and Th2 markers interferon-γ (INF-γ) and interleukin-4 (IL-4) in brain tissue were measured and the INF-γ/IL-4 was calculated. Results: The success rate of ACI reperfusion model was 88.89%. The mental state of rats in the model group was not good, which was improved in the three doses of VT groups after administration. Compared with model group, the neurological function scores of rats in each dose group of VT were significantly decreased 1 d and 3 d after administration (P < 0.05) in a dose-dependent manner. The results of HE showed that the volume of neurons and nucleus of neurons in model group were reduced, and the injury of neurons in VT groups was alleviated after administration, especially in high dose group. Compared with the sham operated group, the damage rates of single and double strand breaks of DNA, INF-γ level and INF-γ/IL-4 in the model group were significantly higher (P < 0.05), while IL-4 level was significantly lower (P < 0.05). Compared with the model group, the rate of DNA single- and double-strand breakage damage, INF-γ level and INF-γ/IL-4 were significantly decreased (P < 0.05) and the level of IL-4 was significantly increased (P < 0.05) in each dose group of VT in a dose-dependent manner. Conclusion: VT has protective effect on nerve function in ACI reperfusion rats, and with the best protective effect at dose of 3.76 mg/kg, which may be related to regulating the balance of Th1/Th2 cells to shift to Th2 and alleviating DNA damage in brain cells.
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Objective: To observe the effect of Ginkgo biloba extract on cerebral cortical ischemia in mice with acute cerebral ischemia and explore its effect on Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) pathway. Methods: Sixty adult healthy male CD1 mice were randomly divided into sham operated group, model group, positive control group (3 × 104 IU/kg ulinastatin) and Ginkgo biloba extract low, medium and high doses (10, 20, 40 mg/kg) groups. The acute cerebral ischemia model in other five groups were all established except sham operated group. After successful modeling, mice in each group were given corresponding drugs iv tail, sham operation group and model group were given the same amount of saline. The pathological changes and histological grades of the cerebral cortex were observed. The survival neuron density of each group was compared. Malondialdehyde (MDA) and superoxide dismutase (SOD) were measured by colorimetry and xanthine oxidation respectively. The expressions of Toll like receptor 4 (TLR4) and nuclear transcription factor NF-κB p65 (NF-κB p65) mRNA were detected by real-time fluorescent quantitative PCR (qRT-PCR). Western blotting was used to detect TLR4 and NF-κB p65 protein expression. Results: In sham-operated group, the structure of cerebral cortex was normal, and the cells were full and arranged tightly and orderly. In the blank control group, the structure of cerebral cortex was severely damaged, and the cells were severely shrunk and disordered. Pathological changes in the Ulinastatin group and Ginkgo biloba extract groups were alleviated and dose-dependent. Compared with the sham operation group, the other five groups showed higher histological grade and MDA level in cerebral cortex (P < 0.05). Compared with the model group, the histological grade and MDA level of cerebral cortex decreased in ulinastatin group and Ginkgo biloba extract groups (P < 0.05). Compared with ulinastatin group, the histological grade and MDA content of brain cortex decreased in high dose group (P < 0.05). Compared with the sham operated group, the density of surviving neurons and the level of SOD in the other five groups decreased (P < 0.05). Compared with the model group, the density of survival neurons and the level of SOD in cortex increased in ulinastatin group and Ginkgo biloba extract group (P < 0.05). Compared with ulinastatin group, the density of survival neurons and the level of SOD in cortex increased in high dose group (P < 0.05). Compared with the sham operated group, the expression of TLR4, NF-κB p65 mRNA and protein in the other five groups increased (P < 0.05). Compared with the model group, the expression of TLR4, NF-κB p65 mRNA and protein in cortex of mice in ulinastatin group and Ginkgo biloba extract group decreased (P < 0.05). Compared with ulinastatin group, the expression of TLR4, NF-κB p65 mRNA and protein in the brain cortex of mice decreased in the high dose group (P < 0.05). Conclusion: Ginkgo biloba extract can alleviate the pathological changes caused by cerebral ischemia in mice with acute cerebral ischemia, alleviate neurological impairment, and improve oxidative stress indexes of cerebral cortex tissues. It is presumed that it may be achieved by regulating TLR4/NF-κB p65 signaling pathway and inhibiting the expressions of TLR4 and NF-κB p65 proteins.
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OBJECTIVE: To observe the effect of scalp-acupuncture intervention on the expression of Interleukin (IL)-10 mRNA, IL-6 mRNA and tumor necrosis factor (TNF) - α in the parahippocampal gyrus of cerebral ischemia (CI) rats, so as to explore its molecular mechanisms underlying improvement of CI. METHODS: A total of 64 male SD rats were randomized into normal control, model, medication and scalp-acupuncture groups (n＝16 rats in each group). The focal CI model was established by middle cerebral artery occlusion. Intraperitoneal injection of Ammonium Pyrrolidine Dithiocarbamate (100 mg•kg－1•d－1) was administrated for rats in the medication group, once a day for 7 days. For rats of the scalp-acupuncture group, the acupuncture needles were rapidly inserted into bilateral Dingnieqianxiexian (MS6), followed by twirling the needles at 100 cycles/min for 1 min, once again every 10 min during 20 min' needle retention. The treatment was conducted once a day for 7 days. The neurologic deficit score (0－4 points, impaired consciousness, death, etc.) and neurological function score (motor, sensory and sensory tests, 0－10 points) were assessed according to Longa's (1989) and Schabitz's (2004) methods, respectively. The expression levels of IL-10 mRNA and IL-6 mRNA were detected by fluorescence quantitative PCR, and the expression of TNF-α was detected by immunohistochemistry. RESULTS: After modeling, the neurologic deficit and neurological function scores and the expression levels of IL-10 mRNA, IL-6 mRNA and TNF-α protein in the parahippocampus were significantly increased in the model group than in the normal control group (P<0.01). Following the intervention, the neurologic deficit and neurological function scores as well as IL-6 mRNA and TNF-α protein expression were significantly down-regulated in both scalp-acupuncture and medication groups (P<0.05), and the expression of IL-10 mRNA was obviously increased (P<0.05) relevant to the model group. CONCLUSION: Scalp-acupuncture can improve neurologic function in CI rats, which is related to its effects in up-regulating the expression of IL-10, then down-regulating the expression of IL-6 and TNF-α (reducing inflammatory response) in the parahippocampal gyrus.
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Objective:To explore the mechanism of Sailuotong capsules in treating acute cerebral ischemia from the perspective of metabonomics. Method:A total of 24 SD rats were randomly divided into 3 groups, including sham-operated group, model group and Sailuotong group (33 mg·kg-1). The rat model of acute multiple cerebral infarction was established by injecting fluorescent microspheres into internal carotid artery. After the successful operation, rats in Sailuotong group were administered by duodenal injection immediately, and the dosage volume was 2 mL·kg-1. Endogenous metabolites in rat brain tissues of each group were determined by UPLC-Q-TOF-MS. The relevant data and biomarkers were analyzed by principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA). Result:The analysis of pattern recognition indicated that the metabolite profiles in model group and sham-operated group were separated obviously, and ten biomarkers related to acute cerebral ischemia were also identified. Compared with the sham-operated group, contents of N-acetylaspartate (NAA), fumaric acid, glutathione, dehydroascorbic acid, aspartic acid and S-adenosylhomocysteine were decreased, while the contents of arginine, citrulline, saccharopine and hydantoin-5-propionic acid were increased in the model group. Meanwhile, the ten abnormal biomarkers mentioned above got restoration in Sailuotong group. Conclusion:The main regulated metabolic pathways of Sailuotong capsules are NAA metabolism, arginine metabolism, energy metabolism, oxidative stress, etc.
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Objective To investigate the value of acoustic radiation force impulse imaging (ARFI) combined with contrast-enhanced ultrasound (CEUS) in diagnosis of acute cerebral ischemia (ACI) in patients with carotid artery vulnerable plaque (VP). Methods One hundred and ten patients with carotid artery VP diagnosed by routine ultrasound admitted to Renhe Hospital Affiliated to Three Gorges University from October 2017 to January 2019 were selected as subjects, including 59 patients with ACI (ACI group) and 51 patients with non-ACI (non-ACI group) confirmed by magnetic resonance imaging (MRI). All patients underwent routine ultrasound, CEUS and ARFI examinations, the differences in sizes of VP, shear wave velocity (SWV) and enhancement intensity (EI) were compared, and the diagnostic values of SWV and EI were evaluated by the analyses of receiver operating characteristic curve (ROC). Results Two hundred and ten VPs were found in 110 patients, including 112 grade 1 plaques, 53 grade 2 plaques, and 45 grade 3 plaques, compared with grade 1 plaques, the proportion of mixed echo (MP) and strong echo (SP) in grade 2 plaques, and the proportion of all echo types in grade 3 plaques were all significantly different from that of grade 1 plaques (all P < 0.05); compared with grade 1 plaques, the proportion of grade 2 plaques with thickness ≤ 2.0 mm, and the proportion of grade 3 plaques with thickness ≤ 2.0 mm and more than 3.1 mm were all significantly different from that of grade 1 plaques (all P < 0.05). SWV in ACI group was obviously lower than that in non-ACI group (m/s: 1.91±0.54 vs. 2.41±0.57), and EI in ACI group was significantly higher than that in non-ACI group (dB: 3.62±1.13 vs. 2.81±1.05), the difference being statistically significant (both P < 0.05). The area under the ROC curve (AUC) of SWV was 0.681 and the cutoff value was 2.21 m/s, sensitivity, specificity, positive predictive value and negative predictive value were 83.05%, 80.39%, 83.05%, 80.39%; the AUC of EI was 0.638, and the cutoff value was 3.71 dB, sensitivity, specificity, positive predictive value and negative predictive value were 79.66%, 74.51%, 78.33%, 76.00%. AUC of SWV combined with EI was 0.812, sensitivity, specificity, positive predictive value and negative predictive value were 93.22%, 94.12%, 94.83%, 92.31%, significantly higher than those of SWV or EI alone (all P < 0.05). Conclusion In ACI patients, the SWV of VP decreases and EI of VP increases, the detection efficacy of SWV combined with EI for diagnosis of ACI has relatively high clinical value, as the combined diagnostic efficiency is significantly higher than that of either SWV or EI alone.
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Objective To investigate the effect of early-stage acupuncture therapy on local glucose metabolism in model rats with cerebral ischemia. Methods Eighty three-month-old SD rats were randomly divided into 4 groups,namely normal group,model group,2-h acupuncture group and 24-h acupuncture group,20 rats in each group. Craniotomy was used to establish the rat model of acute cerebral ischemia. Acupuncture treatment was carried out on acupoint of Baihui(GV20)and Renzhong(DU26)with reducing method,needle twirling and rotating frequency being 120 times per minute,once every other 4 min and for one min,and the total needling time for 30 min. Rats in 2-h acupuncture group were given acupuncture 2 h after the successful modeling,and once again after 24 h,two times in total;rats in 24-h acupuncture group were given acupuncture only for one time 24 h after successful modeling. At the end of treatment,the rat neurological function was scored,and the infarction area was measured by 2,3,5-triphenyltetrazole chloride (TTC)staining. The protein expression levels of glucose transporter(GLUT)1 and 3 in ischemic brain tissue were detected by immunohistochemistry. Results Compared with the normal group, the scores of neurological function in the model group were increased;TTC staining results showed that the left hemisphere was swollen,and the infarct volume was significantly larger than that of the contralateral side;immunohistochemical results showed that the GLUT1 and GLUT3 expression levels in the ischemic brain tissue were increased(P < 0.01). Compared with the model group,2-h acupuncture group and 24-h acupuncture group could effectively improve the cerebral ischemia, reduce the neurological function indexes and infarction area showed by TTC staining,and increase the expression levels of GLUT1 and GLUT3 in ischemic brain tissue significantly (P<0.05). And the therapeutic effect of 2-h acupuncture group was superior to that of 24-h acupuncture group(P<0.05). Conclusion Acupuncture can effectively improve cerebral ischemia in rats with acute cerebral ischemia. Acupuncture can improve the energy metabolism of ischemic brain tissue by up-regulating the protein expression of cerebral GLUT1 and GLUT3 and by increasing the blood-brain barrier transport efficiency for glucose,thus to promote glucose metabolism and provide energy for ischemic brain tissue to relieve relatively inadequate energy, and to protect against cerebral ischemic injury. Early acupuncture intervention exerts a positive effect on regulating energy metabolism of rats with cerebral ischemia.
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OBJECTIVE: To observe the effect of scalp-acupuncture intervention on the expression of parahippocampal factor-κB p 65 mRNA (NF-κB p 65 mRNA), IκB mRNA, interleukin-1 β (IL-1 β) and tumor necrosis factor-α (TNF-α) in rats with cerebral ischemia (CI), so as to investigate its molecular mechanisms underlying improving CI by reducing inflammatory response. METHODS: A total of 64 SD rats were randomized into normal control, model, medication and scalp-acupuncture groups, with 16 rats in each group. The focal CI model was established by middle cerebral artery occlusion (MCAO). Intraperitoneal injection of Pyrrolidine Dithiocarbamate (100 mg•kg－1•d－1) was administrated for rats in the medication group, once a day for 7 days. For rats of the scalp-acupuncture group, the acupuncture needles were rapidly inserted into bilateral Dingnieqianxiexian (MS 6) and Dingniehouxiexian (MS 7), followed by twirling the needles at 200 cycles/min for 1 min, once again every 10 min during 30 min's needle retention. The treatment was conducted once a day for 7 days. The neurologic deficit score (0－5 points, impaired consciousness, death, etc.) and neurological function score (motor, sensory and sensory tests, 0－10 points) were assessed according to Longa's (1989) and Schäbitz's (2004) methods, respectively. The expression levels of NF-κB p 65 mRNA and IκB mRNA in the parahippocampus gyrus tissue were detected by fluorescence quantitative reverse transcription-PCR, and IL-1 β and TNF-α proteins in the parahippocampus gyrus tissue were detected by immunohistochemistry. RESULTS: After modeling, the neurologic deficit and neurological function scores and the expression levels of NF-κB p 65 mRNA, IL-1 β and TNF-α in the parahip-pocampus were significantly increased in the model group than in the normal group (P<0.01), while the expression of IκB mRNA was considerably down-regulated (P<0.01). Following treatment intervention, the neurologic deficit and neurological function scores as well as NF-κB p 65 mRNA, and IL-1 β and TNF-α protein expression were significantly decreased in both scalp-acupuncture and medication groups compared with the model group (P<0.05, P<0.01), and the decreased expression of IκB mRNA was obviously increased (P<0.05)．. CONCLUSION: Scalp-acupuncture can improve neurologic function in cerebral ischemic rats, which is related with its effects in up-regulating the expression of IκB to inhibit the dissociation of NF-κB, then decreasing the expression of IL-1 β and TNF-α (reducing inflammatory response) in the parahippocampal gyrus tissue.
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Brain damage can cause lung injury. To explore the mechanism underlying the lung injury induced by acute cerebral ischemia (ACI), we established a middle cerebral artery occlusion (MCAO) model in male Sprague-Dawley rats. We focused on glia maturation factor β (GMFB) based on quantitative analysis of the global rat serum proteome. Polymerase chain reaction, western blotting, and immunofluorescence revealed that GMFB was over-expressed in astrocytes in the brains of rats subjected to MCAO. We cultured rat primary astrocytes and confirmed that GMFB was also up-regulated in primary astrocytes after oxygen-glucose deprivation (OGD). We subjected the primary astrocytes to Gmfb RNA interference before OGD and collected the conditioned medium (CM) after OGD. We then used the CM to culture pulmonary microvascular endothelial cells (PMVECs) acquired in advance and assessed their status. The viability of the PMVECs improved significantly when Gmfb was blocked. Moreover, ELISA assays revealed an elevation in GMFB concentration in the medium after OGD. Cell cultures containing recombinant GMFB showed increased levels of reactive oxygen species and a deterioration in the state of the cells. In conclusion, GMFB is up-regulated in astrocytes after ACI, and brain-derived GMFB damages PMVECs by increasing reactive oxygen species. GMFB might thus be an initiator of the lung injury induced by ACI.
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Animals , Male , Rats , Brain , Metabolism , Pathology , Brain Ischemia , Pathology , Bronchoalveolar Lavage Fluid , Cell Hypoxia , Physiology , Cells, Cultured , Cerebrovascular Circulation , Physiology , Chromatography, High Pressure Liquid , Culture Media, Conditioned , Pharmacology , Disease Models, Animal , Endothelial Cells , Metabolism , Gene Expression Regulation , Physiology , Glia Maturation Factor , Metabolism , In Situ Nick-End Labeling , Lung Injury , Metabolism , Pathology , Neuroglia , Metabolism , Neurologic Examination , Peroxidase , Metabolism , Proteome , RNA Interference , Physiology , RNA, Small Interfering , Genetics , Metabolism , Rats, Sprague-Dawley , Reactive Oxygen Species , Metabolism , Tandem Mass SpectrometryABSTRACT
En este artículo presentamos el caso de un paciente femenino de 59 años de edad que ingreso al hospital por insuficiencia respiratoria aguda; diagnosticada con trombosis venosa profunda (TVP) y tromboembolia pulmonar (TEP) masiva. Al cuarto día de admisión desarrolló afasia global y hemiplejia derecha. Imagen de resonancia magnética (IRM) del cerebro demuestra un infarto cerebral agudo en el territorio de la arteria cerebral media izquierda. La Ecografía trans-esofágica evidencia un foramen ovale permeable de 1.8 cm de diámetro con una derivación de flujo arterio-venosa de derecha a izquierda significativo. La paciente fue sometida al cierre del defecto cardiaco por cateterismo con resultados favorables sin recurrencia de infartos cerebrales posteriores. También revisamos la literatura sobre embolia paradójica como causa de infartos cerebrales y brindamos algunas recomendaciones para el manejo y prevención de infartos cerebrales criptogénicos.
Herein, we present a case of a 59 years old woman who was admitted to the hospital due to respiratory failure. She was diagnosed with deep vein thrombosis and massive pulmonary embolism. At the fourth day of admission she developed acute onset of global aphasia and dense acute right hemiplegia. Magnetic resonance imaging demonstrates an acute infarct in the left medial cerebral artery territory. Transesophageal echocardiogram found a large patent foramen ovale of 1.8 cm of diameter with a large right to left shunting. Patient underwent to successful closure of the defect via cardiac catheterization with no recurrence of embolic events. We also review the literature of paradoxical embolus as a cause of cerebral infarcts and provide some recommendations for treatment and prevention of cryptogenic infarcts.
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Humans , Female , Middle Aged , Respiratory Insufficiency/complications , Embolism, Paradoxical/diagnosis , Pulmonary Embolism/diagnosis , Venous ThrombosisABSTRACT
Objective:To explore the lactate metabolism in brain tissue of the mice with early acute hypoxia-ischemia injury,and to provide data support for 9.4T 1 H-NMR spectroscopy in detecting the lactate level clinically.Methods:Eighty Kunming mice were randomly divided into sixteen groups (0 s,20 s,40 s,60 s,2 min,4 min, 6 min,8 min, 10 min, 12 min, 14 min, 16 min, 18 min,and 20 min)according to the duration of hypoxia-ischemia (n=5).The changes of lactate levels were detected by 9.4T 1 H-NMR spectroscopy. Results:After the initiation of hypoxia-ischemia injury,the lactate level began to increase rapidly to the highest value of (6.89 ± 0.34)μmol·g-1 at 20 s,then started to decline quickly from 40 s to 2 min,and eventually decreased to a stable level of (4.85±0.36)μmol·g-1 until 6 min.Compared with control group,the levels of lactate in brain tissue of the mice in hypoxic-ischemic groups were increased (P <0.01).Conclusion:40 s of acute hypoxia-ischemia may be the lactate cerebral neuron threshold during the anaerobic glycolysis. 9.4T1 H-MRS can provide the exact time window for detecting the lactate metabolism.
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OBJECTIVE: To observe the neuro-protective effects of harpagide on acute cerebral ischemic injury in mice and its mechanism involving mitochondria. METHODS: Acute cerebral ischemia were achieved by operation of MCAO in the left brain, random allocation was taken to divide ICR mice into sham group, model group, nimodipine group and harpagide (5,10,15 mg·kg-1) groups. Mice were intraperitoneal injected harpagide immediately after surgeiy. Nerve function score, content of brain water, brain index and the common changes of brain pathological structure in HE staining were measured: Ability of mitochondria Ca2+-Mg2+-AT-Pase and protein expression level of caspase-3 in the MCAO mice' brains was determined: Ultrastructure change of mitochondria under the TEM was observed. RESULTS: Compared with model group, the harpagide groups could decreased the nerve function score, the content of brain water, brain index and the volume of ischemia in mice with different degrees in MCAO mice (P-1 of harpagide could increased the activity of Ca2+-Mg2+-ATPase obviously (P<0.01): And significantly decreased the protein expression level of caspase-3 (P<0.01): harpagide groups could protect the pathogeny structure and the ultrastructure of mitochondria with different degrees in MCAO mice, decrease edema of mitochondria obviously. CONCLUSION: Harpagide could obviously protect acute cerebral ischemia in mice, its therapeutical effects are approached to protecting the activity of brain mitochondria and decreasing protein expression level of caspase-3.
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Objective To observe the effect of scalp needling at different time points on focal cerebral microcirculation in rats with focal ischemia and reperfusion ( I-R). Methods One hundred SD rats were randomized into normal group, sham operation group, model group and scalp needling group. The model group and scalp needling group were divided I-R 12, 24, 48 and 72 h subgroups according to the time of ischemia and reperfusion, 10 rats in each subgroup. The normal group had no oper ation, sham operation only had the operation for vessel isolation, and model group and scalp needling group received middle cerebral artery occlusion with thread. Scalp needling group also had electro-acupuncture on scalp points along vertex and temple anterior linea oblique and posterior linea oblique. And then we observed the neurological severity scores (NSS) and detected the cerebral blood flow ( CBF) in the focal ischemic brain with laser Doppler blood stream meter before I-R and 12, 24, 48 and 72 h after I-R. Immunofluorescence method was used for counting the focal ischemic cerebral microvascular endothelial cells, and then the correlation of cerebral microvascular endothelial cells count with the cerebral blood flow volume was evaluated with Pearson correlation analysis. Results NSS in scalp needling group was lower than that in the model group (P0.05). Except for reperfusion for 24 hours, CBF in scalp needling group was higher than that in the model group at different time points ( P<0.05 or P<0.01). Microvascular endothelial cells count in scalp needling group was higher than that in the model group after reperfusion for 24, 48 and 72 hours ( P<0.05 or P<0.01). In the model group and scalp needling group, cerebral blood flow volume was positively correlated with microvascular endothelial cells count. Conclusion Scalp needling shows obvious effect on improving the microcirculation, increasing CBF and cerebral microvascular endothelial cells count, and promoting the recovery of ischemic tissues of rats after I-R.
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A case of "spontaneous" acute subdural hematoma caused by aspirin and plavix therapy has not been described previously. As an isolated cerebrovascular event related to aspirin and plavix therapy, this is the first report described in the literature. It also represents a new differential diagnosis for nontraumatic acute subdural hematomas.
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Humans , Aspirin , Diagnosis, Differential , Hematoma, Subdural, Acute , TiclopidineABSTRACT
A prospective study including 70 patients with acute cerebral infarction at Hospital 108 from July 2004 to Jun 2005. Results: Increasing blood glucose level is very common among acute stroke patients accounting for 54.3%. Blood glucose level due to response during acute stroke is commonly within the range of 7 – 10mmol/l (50%). There are reverse correlations between blood glucose and Glasgow, Herry and Barthel scores. HbA1c is essential to differentiate hyperglycemia due to diabetes or response
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@#ObjectiveTo approach effects of acupuncture on ganglioside in rats with acute cerebral ischemia.Methods204 Wistar rats were randomly divided into the normal group, model group, acupuncture group and medicine group, and middle cerebral artery embolism has been made by thread-ligation method in the latter three groups. Ganglioside content in the rat brain had been measured respectively after cerebral ischemia 1,2,3,5,7,12 and 24 hours.ResultsThe content of lipid-bound sialic acid (LBSA) has decreased significantly after the acute cerebral ischemia, but LBSA contents of the acupuncture group and medicine group were higher significantly than that of the model group, and these two groups have been similar in curative effect, and have difference only at embolism 2,3 and 5 hours.Conclusion Acupuncture can regulate ganglioside and play the role of cerebral protection and neuroplasticity.
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@#ObjectiveThe research is that pulse magnetic acupuncture in scalp point affects the nerve function and endothelin-1(ET-1)capacity of acute cerebral ischemia rat. Methods70 rats were divided randomly into seven groups: normal, artificial operation, model, static magnetic acupuncture, normal acupuncture, electric acupuncture and pulse magnetic acupuncture, every group had 10 rats and the nerve function and plasma ET-1 capacity of rats were examined.ResultsStatic acupuncture, electric acupuncture, pulse magnetic acupuncture and normal acupuncture can improve the nerve function and decrease the capacity of ET-1, but pulse magnetic acupuncture and normal acupuncture improve obviously.Conclusions Pulse magnetic acupuncture and normal acupuncture have the same effect to improve the nerve function and decrease the capacity of ET-1.
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Objective To investigate the neuroprotective effects of phycocyanin injection by internal carotid artery in acute cerebral ischemic reperfusion in rats.Methods The model of middle cerebral artery occlusion reperfusion(MCAO/R) was established using the intraluminal filament occlusion with 84 healthy adult male Wistar rats,and treated by phycocyanin injection through internal carotid artery.The nervous function scores,brain water content,cerebral infarction volume and cell apoptosis in brain tissues and the phycocyanin effects on above indexes were measured respectively.Results The rats showed some extent of neurobehavioral function disorders after ischemic reperfusion.In phycocyanin group rats,the nervous function scores,brain water content,cerebral infarction volume and the number of apoptotic cells in cortex,striatum and hippocampus reduced significantly compared to the model group.Conclusion phycocyanin injection through internal carotid artery showed obvious neuroproctective effects in acute cerebral infarction in rats.
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The development of postischemic irreversible brain damage depends upon the length of ischemia and its severity during arterial occlusion, although release of the occlusion always leads to restoration of normal or above noraml cerebral blood flow. The experiment was planned to determine the effects of mannitol on cerebral ischemia on subsequential regional cerebral blood flow(rCBF) and somatosensory evoked potential(SEP) following reperfusion after ischemia and also define the proper time of vascular occlusion without irreversible brain damage. Cerebral ischemia was induced in cat by transorbital occlusion of the left MCA with a Sugita clip for period of 30 minutes and the ischemic brain was reperfused for 180 minutes by removing the clip. Forty adult cats, weighing 2.5 to 4.0 Kg were divided into 5 group ; control(Group I, n=8), permanent MCA occlusion(Group II, n=8), permanent MCA occlusion with mannitol infusion(Group III, n=8), permanent MCA occlusion with mannitol infusion(Group III, n=8), 30 minutes MCA clipping followed by reperfusion(Group IV, n=8) and 30 minutes MCA clipping with mannitol infusion followed by reperfusion groups(Group V, n=8) respectively. The rCBF and SEP measurents were carried out in each animal immediately, after MCA occlusion, at 30 minutes, 60 minutes, 90 minutes, 120 minutes, 150 minutes and 180 minutes followed by perfusion. The rCBF was measured by the hydrogen clearance technique. Mannitol was given in bolus of lg/kg body weight as a 25% solution delivered via the femoral vein. The results were as follows : 1) Gradual elevation of intracranial pressure(ICP) and systolic blood pressure were observed after MCA occlusion. Treatment with mannitol in MCA occlusion animals(Group III & V) decreased ICP immediately after infusion of mannitol. 2) Normal control rCBF(ml/100 g/min) were 51.94+/-5.05 in the left temporal(LT) and 50.80+/-4.87 in the left perietal lobes(LP). 3) The MCA occlusion resulted in a reduction of the blood flows to 72% of the normal control ones(LT : 14.29+/-4.81 ml/100 g/min) at the left temporal area immediately after occlusion and also a reduction of flows to 80.4% of the normal control ones(LT : 10.24+/-3.69 ml/100 g/min) at 180 minutes after occlusion in Group II. 4) In the mannitol-treated group(group IV), reperfused animals, with removal of the clip on MCA had an improved postischemic recovery of blood flow and ipsilateral cerebral blood flows were restored to 42.5% of the normal control ones(LP : 21.2+/-4.13 ml/100 g/min) at 180 minutes after occlusion in Lt. parietal CBF. 5) In the reperfusion group(group IV), reperfused animals, with removal of the clip on MCA had an increase in rCBF to the level of 83.3% of the control value(LT : 45.78+/-6.80 ml/100 g/min) at 180 minutes after reperfusion and also reperfused animals, with treated mannitol had further increase the blood flow up to the level of 92.5% of the control value(LT : 49.04+/-43.6 ml/100 g/min) at 180 minutes after reperfusion. 6) After the MCA occlusion, the SEP was present but markedly altered in shape and particularly the early components of the SEP were suppressed in the ipsilateral occlusion hemisphere. 7) In the mannitol-treated reperfusion group(Group V) the amplitude of the SEP was restored to 80% of control value. The SEP was significantly suppressed if the rCBF fell below 10-14 ml/100 g/min. These result suggest that provided CBF can be restored to above the 40% threshold well within 30 minutes, prevention of ischemic brain damage can be expected and also the mannitol may of benefit in prolongation of the time threshold for the formation of the cerebral ischmia after vessel occlusion.
Subject(s)
Adult , Animals , Cats , Humans , Blood Pressure , Body Weight , Brain , Brain Ischemia , Evoked Potentials , Femoral Vein , Hydrogen , Ischemia , Mannitol , Perfusion , Rabeprazole , ReperfusionABSTRACT
Objective To observe the interference actien of Buqi Huoxue Decoction(Herbal decoction for reinforcing qi and activating blood)on the model rats with acute cerebral ischemia.Methods Sixty SD rats were randomized into 6 groups,i.e.sham operation group,model group,nimodipine group,and Buqi Huoxue Decoction groups of high,middle,and low dosages,with 10 rats in each.Except the model and sham operation groups,the others were given Buqi Huoxue Decoction through intragastric gavage for 5 days.The acute cerebral ischemia models were made on the sixth day.One hour before modeling,the last medication was applied.At the time point 6h,12h,and 24h,the blood sample was taken from the aorta abdominalis for detecting the tumor necrosis factor-?(TNF-?).After 24h,the hemorheology test was performed.Results Compared with the model group,the whole blood viscosity including the high shear rate and low shear rate and erythrocyte aggregation index of the Nimodipine group and Buqi Huoxue Decoction groups of high and middle dosages were lowered(P