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1.
AIM: To observe the change of L-type voltage-gated Ca2+ channel current during focal brain ischemia in the normal rats and the rats with diabetes mellitus (DM). METHODS: Combination of high-fat diet with streptozotocin (STZ) was used to establish DM animal model. The operation of middle cerebral artery occlusion (MCAO) with monofilament on the rats was performed. The animals were divided into sham operation group, MCAO 1 h group, MCAO 3 h group, MCAO 6 h group, MCAO 24 h group, DM sham operation group, DM+MCAO 1 h group, DM+MCAO 3 h group, DM+MCAO 6 h group and DM+MCAO 24 h group. The score of neural function was determined to judge the degree of palsy in the rats in MCAO 24 h group and DM+MCAO 24 h group. The changes of L-type voltage-gated Ca2+ channel current of cortex neurons during ischemia were measured using the whole-cell patch clamp technique. RESULTS: The rats in DM+MCAO 24 h group awaked slowly, and the degree of semiplegia was more serious than that in the rats in MCAO 24 h group. The score of neural function in DM+MCAO group was higher than that in MCAO group (P<0.05). The longer the ischemic time was, the higher L-type voltage-gated Ca2+ channel current was observed in MCAO group and DM+MCAO group (P<0.05). L-type voltage-gated Ca2+ channel current in DM+MCAO group was higher than that in MCAO group at each time point(P<0.05). CONCLUSION: The aggratation of ischemic injury during DM+MCAO is probably associated with Ca2+ overload induced by calcium channel opening and current increasing. 相似文献
2.
AIM: To observe the neuroprotective effect of combined treatment with taurine and diazepam against focal cerebral ischemia-reperfusion in rats. METHODS: Sixty male Sprague-Dawley rats were randomly divided into five groups: sham-operation group, vehicle group, taurine group (200 mg/kg, ip), diazepam group (10 mg/kg, ip) and combined treatment group (taurine 100 mg/kg+diazepam 5 mg/kg). Focal cerebral ischemia was induced by the method of middle cerebral artery occlusion (MCAO) in rats, and reperfusion was emerged by removing the thread 2 h later. The drugs were administered respectively at the time of reperfusion, and subsequently repeated once 12 h later. The animals in vehicle group were intraperitoneally injected with isodose normal saline. The neurological deficit score, the brain water content and cerebral infarction were measured 48 h after MCAO. Other 5 group animals of focal cerebral ischemia-reperfusion (n=16 in each group) were set up as mentioned above and accepted treatments 10 h after reperfusion, likewise repeated once 12 h later. Twelve animals in each group were adopted the same management as the previous 5 groups at 48 h after MCAO. The remained 4 animals in each group were sacrificed until two weeks after MCAO to observe the histopathological changes by nissl staining. RESULTS: Compared to vehicle group, the animals in combined treatment group at 2 h or 12 h after MCAO both decreased the neurological deficit score, reduced the brain water content and infarct volume (P<0.01 or P<0.05). The combined treatment significantly alleviated the neurological necrosis as well. The neuroprotective effect of the combined treatment was superior to that of using taurine or diazepam alone. CONCLUSION: These results suggest that combination of taurine and diazepam treatment has a coordinate neuroprotective effect on both the acute and chronic brain damage of focal cerebral ischemia-reperfusion. 相似文献
3.
AIM: To explore the mechanism of 3-nitropropionic acid (3-NPA) preconditioning that induces cerebral ischemic tolerance in rats by affecting the expression of brain-type glucose transporters (GLUT1 and GLUT3) at mRNA and protein levels in cerebral tissues.METHODS: The male SD rats were used in the experiments and divided randomly into sham operation group (sham group, n=4), control group of 3-NPA preconditioning (3-NPA group, n=4), cerebral ischemia group (M group, n=16) and 3-NPA preconditioning group (IPC group, n=16). M group and IPC group were further divided into 4 subgroups according to the different reperfusion time(4 h, 12 h, 24 h and 48 h). All rats were killed at the corresponding time points. The cerebral tissues in the ischemic side (left) and coronal intermediate 1/3 of cortex were collected. The protein levels and mRNA expression of GLUT1 and GLUT3 were determined by Western blotting and RT-PCR. RESULTS: Compared with M group, the ischemic reperfusion and 3-NPA preconditioning induced the upregulation of GLUT1 and GLUT3 at protein levels with significant differences (F=5.848, P<0.05 and F=6.295, P<0.05, respectively), especially after ischemia-reperfusion for 48 h. The mRNA expression of GLUT1 in IPC group began to increase at 4 h, peaked at 48 h after reperfusion, with significant difference as compared to M group at the corresponding reperfusion time points in each group or sham group. In contrast, the mRNA expression of GLUT3 in IPC group increased at 24 h, and was the highest at 48 h as compared to cerebral ischemia group at the corresponding reperfusion time points or sham group.CONCLUSION: 3-NPA preconditioning increases the expression of GLUT1 and GLUT3 at protein and mRNA levels to maintain the energy supply in brain tissues, indicating a cerebral protective mechanism. 相似文献
4.
AIM: To study rat astrocyte proliferation in ipsilateral hippocampus following focal cerebral ischemia. METHODS: Ischemia was induced by temporary middle cerebral artery occlusion (MCAO). In hippocampus of rats at 3, 7 and 30 days after MCAO, the numbers and anatomic distribution of glial fibrillary acidic protein (GFAP) were detected by immunohistochemistry. The protein expression of GFAP and proliferating cell nuclear antigen (PCNA) in the ipsilateral hippocampus were analyzed by Western blot analysis. RESULTS: Astrocytes appeared hypertrophic, with increased process thickness and numbers at 7 days after MCAO, and the highest density of astrocytes were seen at 30 days in the CA1, CA2 regions of the ipsilateral hippocampus. Western blot analysis revealed that GFAP levels were normal at 3 days, but increased by 7 days and remained elevation at 30 days. Western blot analysis of PCNA protein also revealed identified upregulation PCNA at 3 days after MCAO and the expression peaked at 7 days. CONCLUSION: This study demonstrates that focal cerebral ischemia in the rat results in a rapid response, a process often referred to as reactive astrogliosis or glial scarring, from resident astrocytes of the ipsilateral hippocampus to the side of ischemia. 相似文献
5.
AIM: To investigate the effects of astragaloside IV (AS-IV) on autophagy in rats with cerebral ischemia/reperfusion (I/R) injury. METHODS: The focal cerebral ischemia/reperfusion of rat left middle cerebral artery occlusion (MCAO) was induced by suture method. Male SD rats (n=70) were randomly divided into sham operation group, I/R group, solvent control group, AS-IV group, AS-IV+autophagy inhibitor (3-methyladenine, 3-MA) group, 3-MA group and autophagy activator (rapamycin, Rapa) group. Except for sham operation group, the rats in other groups were subjected to ischemia for 2 h and reperfusion for 24 h. The rats with successful modeling were selected according to Zea Longa scoring criteria. The volume of cerebral infarction was measured by TTC staining. The morphological changes of nerve cells in the rats were observed with Nissl staining. The phenomenon of autophagy was observed under transmission electron microscope. The protein expression of beclin-1 and LC3-Ⅱ was determined by Western blot. RESULTS: No neurological deficit in sham operation group was observed, and the cerebral infarction was not found. Compared with sham operation group, obvious cerebral infarction was observed, the Nissl bodies were small in size and number and stained light, typical autophagosomes were observed, and the protein expression of beclin-1 and LC3-Ⅱ was increased in I/R group (P<0.05). Compared with I/R group, the volume of cerebral infarction was decreased obviously, neurological deficit restored significantly, and the number of autophagosomes and the protein expression of beclin-1 and LC3-Ⅱ were increased in AS-IV group and Rapa group (P<0.05). However, no significant difference between solvent control group and I/R group was observed (P>0.05). Compared with AS-IV group, the neurological deficit was serious, the volume of cerebral infarction and the number of autophagosomes were increased, while the expression of beclin-1 and LC3-Ⅱ was decreased in AS-IV+3-MA group and 3-MA group (P<0.05). CONCLUSION: Astragaloside IV may play an important role in atte-nuating cerebral ischemia/reperfusion injury by activating autophagy. 相似文献
6.
AIM: To study the role of autophagy-related gene 5 (Atg5) in cerebral ischemia and reperfusion injury in mice. METHODS: BALB/c male mice (weighing 18~22 g) were randomly divided into sham group, ischemia/reperfusion (I/R) group, Atg5 siRNA group and control siRNA group. Focal cerebral ischemia was performed using the method of middle cerebral artery occlusion (MCAO) for 60 min and reperfusion for 24 h. In siRNA group and control group, 5 μL Atg5 siRNA or scrambled siRNA was administered by intracerebroventricular injection 24 h before MCAO. The expression of Atg5 at mRNA and protein levels in ischemic cortex at 24 h after reperfusion was determined by real-time PCR and Western blot. The infarct volume and edema were evaluated by TTC staining, and motor deficits were evaluated by neurological scoring. RESULTS: The expression of Atg5 at mRNA and protein levels was significantly increased 24 h after reperfusion in I/R group compared with sham group. Atg5 siRNA obviously decreased the expression of Atg5 at mRNA and protein levels induced by I/R. Inhibition of Atg5 exacerbated the infarct volume and ameliorated the neurological symptoms. CONCLUSION: Atg5 has neuroprotective effect on focal cerebral ischemia and reperfusion injury. 相似文献
7.
SHE Yan HU Yu-qin ZHANG Jin HAO Yu-xing CAI Yuan ZHANG Guo-guo WANG Rui-zhi DENG Chang-qing LIU Xing-chun 《园艺学报》2019,35(8):1379-1386
AIM:To investigate the changes of pyroptosis in hippocampus and cortex at different time points after cerebral ischemia-reperfusion, and to explore its mechanism from NLRP3-mediated classical pyroptosis pathway, and to analyze the role of pyroptosis in different parts of cerebral injury. METHODS:SD rats were randomly divided into sham operation group (sham group) and model group (MCAO/R group). The rats in model group was further divided into cerebral ischemia-reperfusion 6 h group (MCAO/R 6 h group), 12 h group (MCAO/R 12h group)and 24 h group (MCAO/R 24 h group). The rat model was established on rats by middle cerebral artery occlusion and reperfusion (MCAO/R) induced by modified right-side thread method. Neurologic function score, 2, 3, 5-triphenyltetrazolium chloride (TTC) staining and morphological observation were used to evaluate the degree of nervous cell injury. TUNEL and caspase-1 immunofluorescence double staining were used to detect pyroptosis. The protein expression of NLRP3, cleaved caspase-1, pro-caspase-1 and interleukin-1β (IL-1β) was determined by Western blot. RESULTS:Neurological damage occurred at different times after cerebral ischemia-reperfusion. TTC staining showed that the volume of cerebral infarction gradually increased with the prolongation of reperfusion time (P<0.05). The hippocampal CA1 area and cortical area showed typical morphological features such as loose tissue structure, interstitial edema, disordered arrangement of nerve cells, deepening of nucleus staining, nuclear fragmentation and decreased cell number. Immunofluorescence double staining showed that there was a phenomenon of pyroptosis at different time after cerebral ischemia-reperfusion. The pyroptosis of hippocampal CA1 and cortical area was most obvious at 12 h and 24 h after reperfusion (P<0.05). Western blot analysis showed that the expression of NLRP3, cleaved caspase-1, pro-caspase-1 and IL-1β in NLRP3-mediated classic pyroptosis pathway was regulated in different degrees after cerebral ischemia-reperfusion. The protein expression of NLRP3 in hippocampus was significantly increased at 12 h and 24 h after reperfusion (P<0.05), and the protein expression of NLRP3 in cortex was significantly increased at 6 h after reperfusion (P<0.05). The protein expression of pro-caspase-1 in hippocampus was significantly increased at each time points of reperfusion (P<0.05), and the protein expression of pro-caspase-1 in the cortex was significantly increased at 24 h after reperfusion (P<0.05). The protein expression of cleaved caspase-1 in the hippocampus was significantly increased at 12 h after reperfusion (P<0.05), and increased in the cortex at 24 h after reperfusion (P<0.05). The protein expression of IL-1β in the hippocampus was significantly increased at 24 h after reperfusion (P<0.05), and increased in the cortex at 6 h after reperfusion (P<0.05). CONCLUSION:Pyroptosis is involved in neuronal injury after cerebral ischemia-reperfusion. The classic pyroptosis pathway plays an important regulatory role in hippocampus and cortex, especially in hippocampus, suggesting that hippocampus is the main part of secondary nerve impairment induced by pyroptosis and inflammation after cerebral ischemia-reperfusion. 相似文献
8.
AIM: To evaluate the effect of aminoguanidine (AG) on inflammatory factors and neuronal apoptosis after focal cerebral ischemic injury in rats and the possible mechanism of protective effect of AG against cerebral ischemic injury.METHODS: Thirty male SD rats (weighing 250 g-280 g) were randomly divided into three groups: (1) sham operated group (SH group,n=10),(2) ischemic groups (IS group,n=10),(3) AG group (n=10).In AG group,AG at dose of 100 mg·kg-1 was given intraperitoneally twice a day for 3 consecutive days.In IS group,normal saline was given instead of AG.Focal cerebral ischemia was produced by middle cerebral artery occlusion (MCAO) for 12 h.A nylon thread with rounded tip was inserted into left internal carotid artery cranially until resistance was felt.The distance from bifurcation of common carotid artery to the tip of the thread was about 18-19 mm.Focal cerebral ischemia was confirmed by left Horners syndrome and right side hemiplegia.In SH group,the carotid artery was exposed but no thread was inserted.The expression of tumor necrosis factor-α(TNF-α) was determined by immunochemistry and the content of interleulin-1β(IL-1β) was measured by radioimmunoassay.The expressions of Bcl-2 and Bax protein were detected by flow cytometry.RESULTS: The expression of TNF-α and the content of IL-1β were markedly increased after MCAO.Significantly increased DNA fragmentation,the indication of apoptosis,was detected after MCAO.The expression of TNF-α and the content of IL-1β were significantly lower in AG group than those in IS group.The percentage of apoptosis cells and expression of Bax protein were markedly lower in AG group than those in IS group but still significantly higher than those in SH group.The expression of Bcl-2 protein was markedly higher in AG group than that in IS group.No significant difference in the expression of Bcl-2 protein between IS and SH group was observed.CONCLUSION: AG inhibits the increase in the expression of TNF-α and the content of IL-1β,and protects neurons from apoptosis induced by focal cerebral ischemia through increasing the Bcl-2 protein expression and inhibiting the Bax protein expression. 相似文献
9.
AIM: To explore the effects of ghrelin on the brain edema, the permeability of blood-brain barrier (BBB) and the expression of aquaporin 4 (AQP4) after cerebral ischemia/reperfusion in rats. METHODS: Adult male Sprague-Dawley rats were randomly divided into sham operation group, middle cerebral artery occlusion (MCAO) group and ghrelin treatment group. The MCAO model was made with nylon thread for 2 h of occlusion following 22 h of reperfusion. Ghrelin at a dose of 10 nmol/kg was injected via femoral vein at the beginning of reperfusion. The cerebral infarct volume was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Brain functional deficits were evaluated by determining the neurological scores. The changes of brain swelling and water content were analyzed through volume calculation and dry/wet weight measurement. The permeability of BBB was detected by collecting extravascular Evans blue (EB) in the brain cortex. The changes of AQP4 expression were assessed by the methods of immunohistochemistry and Western blotting. RESULTS: Compared with MCAO group, the rats in ghrelin treatment group had smaller brain infarct volume, lower EB exudation content and neurological scores. The percentage of brain swelling, water content and AQP4 expression were lower in ghrelin treatment group than those in MCAO group. CONCLUSION: Ghrelin reduces the injury of cerebral ischemia/reperfusion, and lightens the brain edema and BBB damage in rats. Ghrelin also inhibits the expression of AQP4 in brain tissue. 相似文献
10.
AIM: To investigate the effects of ginsenoside RH2 (GS-RH2) on neovascularization of rats with middle cerebral artery occlusion (MCAO) and its potential mechanisms. METHODS: SPF Sprague-Dawley rats were randomly divided into sham operation (sham) group, MCAO model (MCAO) group and GS-RH2 group, with 18 rats in each group. After surgery, the general condition and neurological function score of the rats were assessed. At the 1st day, 3rd day and 7th day after intervention, the microvessel density (MVD), the content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were examined. The protein expression of kelch-like ECH-associated protein 1 (Keap1), nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was determined by Western blot. RESULTS: Compared with sham group, the rats in MCAO group showed significant neurobehavioral obstacles and ischemic brain infarction with higher neurological function score, while treatment with GS-RH2 significantly improved behavioral impairment and reduced the infarction volume with lower neurological function score. The MVD score in GS-RH2 group was increased as the animal survival time prolonged, while the MVD score in MCAO group was decreased. After intervention for 7 d, the MVD score in GS-RH2 group was significantly higher than that in MCAO group (P<0.05). Compared with sham group, the content of MDA was increased and the activities of SOD and GSH-Px were decreased in MCAO group at each time point. After intervention for 7 d, the MDA content was decreased and the SOD and GSH-Px activities were increased in GS-RH2 group compared with MCAO group. After intervention for 7 d, the protein expression of Nrf2 and HO-1 was increased, while the protein expression of Keap1 was decreased in GS-RH2 group compared with MCAO group(P<0.05). CONCLUSION: Ginsenoside RH2 promotes neovascularization of MCAO model rats. The mechanism may be related to the activation of Keap1/Nrf2 signaling pathway, promotion of the antioxidant enzyme activity and inhibition of oxidative stress. 相似文献
11.
AIM: To explore the effect of complement on the cerebral ischemia/reperfusion injury in rat and the protection by sCR1-SCR15-18. METHODS: 75 male SD rats were randomly divided into three groups: sham operation group (SO, n=15), middle cerebral artery occlusion and reperfusion (MCAO) without treatment group (I/R, n=30); MCAO treated with sCR1-SCR15-18 group (sCR1-SCR15-18, n=30). After the MCAO for 2 h, then reperfusion for 24 h, the scores of neural behavioral functional deficits were determined. Infarction area was measured by TTC staining. Activity of MPO in cerebral cortex was detected. C3b deposition and pathological change were observed by immunohistochemial staining and HE staining, respectively. RESULTS: After reperfusion for 24 h, the neurological deficits score, infarction area and activity of MPO in sCR1-SCR15-18 group were decreased compared to I/R group. In sCR1-SCR15-18 group, C3b deposition in ischemic area was decreased and pathological injury was improved compared to I/R group. CONCLUSION: Complement plays a role in cerebral ischemia-reperfusion injury and sCR1-SCR15-18 exerts a protective effect by inhibiting the excessive activation of complement. 相似文献
12.
AIM: To investigate the effect of Astragalus injection on the expression of apoptotic protease-activating factor 1 (Apaf-1) in the hippocampus of global cerebral ische-mia-reperfusion rats. METHODS: Male SD rats were randomly divided into 4 groups with 30 each: sham operation group, cerebral ischemia-reperfusion group, cerebral ischemia-reperfusion+Astragalus injection group, and cerebral ischemia-reperfusion+vehicle group. The global cerebral ischemia-reperfusion model of the rats was established by 4-vessel occlusion. The rats in cerebral ischemia-reperfusion group, cerebral ischemia-reperfusion+Astragalus injection group and cerebral ischemia-reperfusion+vehicle group were further divided into 7 subsets, according to the reperfusion time of 0 h, 0.5 h, 2 h, 6 h, 24 h, 72 h and 120 h. After reperfusion, the brains were removed at the corresponding time points. The protein expression of Apaf-1 in hippocampal neurons was detected by immunohistochemistry and Western blotting. The mRNA expression of Apaf-1 was observed by RT-PCR. RESULTS: Compared with sham operation group, the expression of Apaf-1 at mRNA and protein levels at all time points except 0 h and 120 h increased obviously in cerebral ischemia-reperfusion group (P<0.05). Compared with cerebral ischemia-reperfusion group, the expression of Apaf-1 at mRNA and protein levels at all time points except 0 h and 120 h decreased obviously in cerebral ischemia-reperfusion+Astragalus injection group (P<0.05). However, those in cerebral ischemia-reperfusion+vehicle group had no obvious change (P>0.05). CONCLUSION: Astragalus injection inhibits the expression of Apaf-1 at mRNA and protein levels in hippocampus of global cerebral ischemia-reperfusion rats, thus inhibiting the apoptosis of hippocampal neurons. 相似文献
13.
AIM:To study the effect of intermittent hypobaric hypoxia preconditioning (IHHP) on the expression of neuroglobin (Ngb) and Bcl-2 in hippocampal CA1 region in the rats with global cerebral ischemia-reperfusion. METHODS:The Wistar rats were randomly divided into sham group, IHHP control group, global cerebral ischemia-reperfusion group (I/R group), and IHHP+I/R group. The 4-vessel occlusion rat model of Pulsinelli was performed in the rats in I/R group and IHHP+I/R group, in which the common carotid artery was occluded for 8 min before reperfusion. Thionine staining and immunohistochemical staining were used to observe the histological changes of the hippcampus and the expression of Ngb and Bcl-2 in the hippocampal CA1 region. RESULTS:A significant increase in the quantity of surviving cells in the hippocampal CA1 region was observed in IHHP+I/R group as compared with I/R group. There was a significant increase in the expression of Ngb and Bcl-2 in the hippocampal CA1 region in IHHP+I/R group as compared with I/R group. CONCLUSION: Through the up-regulation of hippocampal Ngb and Bcl-2 expression, intermittent hypobaric hypoxia preconditioning may play a role in neuroprotection by reducing hippocampal neuronal apoptosis from ischemia-reperfusion. 相似文献
14.
AIM: To identify the proteins interacted with conventional protein kinase Cγ (cPKCγ) which are involved in hypoxic preconditioning (HPC), and to investigate the role of cPKCγ-interacted heat-shock protein 60 (HSP60) in the development of HPC and ischemia (I).METHODS: Healthy male BALB/c mice were randomly divided into normoxia(Norm) and HPC groups. Based on whether middle cerebral artery occlusion (MCAO) was performed, the mice were divided into Norm+sham group, Norm+I group, HPC+sham group and HPC+I group ( all n=6). Immunoprecipitation, two-dimensional electrophoresis and mass spectrometry were applied to identify the proteins interacted with cPKCγ. The changes of HSP60 expression in the brain of the mice after HPC and MCAO were analyzed by Western blotting.RESULTS: The interaction of cPKCγ and HSP60 was confirmed by co-immunoprecipitation result. Compared with Norm groups, the expression level of cPKCγ-interacted HSP60 obviously increased in particulate fraction of cerebral cortex in HPC mice. In the MCAO ischemic animals, the level of HSP60 expression was significantly higher in ischemic core and penumbra in Norm+I group and HPC+I group than that in Norm+sham group. HSP60 expression in ischemic core was lower in HPC+I group than that in Norm+I group.CONCLUSION: cPKCγ-HSP60 signal pathway might be involved in the development of cerebral hypoxic preconditioning in MCAO mice. 相似文献
15.
AIM: To explore the protective effects of atorvastatin on blood brain barrier(BBB) in cerebral ischemia-reperfusion(IR) injury and the potential mechanisms involved. METHODS: SD rats were divided into sham group, IR group and atorvastain group. Intraluminal suture method was used to establish cerebral IR model, and the ischemic brain was reperfused for 72 h after the occlusion. The rats in atorvastatin group were administered with atorvastatin(20 mg·kg-1·d-1) by gavage once a day for 3 consecutive days after operation. At 72 h after reperfusion, neurological function scores, the water content of the brain tissue, Evans blue(EB) content of ischemic hemisphere, the expression of tight junction(TJ)-associated protein occludin and inflammation factor phosphatidylinositiol 3-kinase-p110 gamma(PI3K-p110γ) were tested and analyzed. RESULTS: In IR group, the rats showed elevated neurological function scores(P<0.01), brain tissue water content(P<0.01) and EB content(P<0.01), accompanied with the down-regulation of occludin expression(P<0.01) and up-regulation of PI3K-p110γ(P<0.01) at 72 h after reperfusion. Compared with IR group, decreased brain edema(P<0.01) and EB leakage(P<0.01) were observed in atorvastatin group, accompanied with increased occludin expression(P<0.01) and decreased PI3K-p110γ expression(P<0.01). However, no statistical difference of the neurological function scores between the 2 groups was observed. CONCLUSION: Atorvastain attenuates cerebral IR injury, which may be associated with the inhibition of inflammatory reactions and the up-regulation of TJ-asso-ciated proteins to maintain the stability of BBB. 相似文献
16.
17.
WANG Shu-qiu CONG A-peng LI Yong-yi FU Chun-fang ZHANG Jian-hua WANG Shu-xiang LU Ya-zhen 《园艺学报》2006,22(2):352-354
AIM: To observe the effect of ischemic preconditioning on contents of cytochrome C and mitochondrial calcium in rats after focal cerebral ischemic-reperfusion. METHODS: Focal cerebral ischemic model was made by occlusion of right middle artery in Wistar rats (ischemia for 2 h and reperfusion for 4 h). Rats were randomly divided into three groups: ischemia pretreatment, model and sham operation. Rats in ischemic pretreatment group were undergone transient ischemic preconditioning (30 min) and reperfusion (72 h). The contents of cytochrome C were measured according to Zhangjuntian's improved methods. The contents of mitochondrial calcium were detected by flame atom absorption. RESULTS: The contents of mitochondrial cytochrome C and calcium in model group were significantly lower than those in sham operation (P<0.05, P<0.01), whereas the contents of plasma cytochrome C were markedly higher (P<0.05, P<0.01). The change in ischemic pretreatment group was obviously difference as compared with the model group. CONCLUSION: Ischemic preconditioning reduces the release of mitochondrial cytochrome C and maintain mitochondrial calcium homeostasis. 相似文献
18.
AIM: The present study was designed to examine the changes in glial fibrillary acidic protein (GFAP) expression during cerebral ischemia and the effects of ginkgolide B on GFAP expression. METHODS: The focal thrombotic cerebral ischemia was formed by photochemistry-induced in tree shrews. GFAP stained by ABC immunohistochemistry and absorbance were measured with image analyze system. RESULTS: GFAP expression in astrocytes increased significantly (P<0.01) at 24 h and kept in higher level at 72 h (P<0.01) within penumbra after focal cerebral ischemia. GFAP expression declined when the animals were given GB at 6 h after thrombotic cerebral ischemia. CONCLUSIONS: Neuronal necrosis resulted in GFAP expression in astrocytes after local cerebral ischemia and GB protected neurons by antagonizing PAF receptor and inhibiting GFAP expression. 相似文献
19.
AIM: To investigate the effect of apigenin on the expression of vascular endothelial growth factor (VEGF) in the rats under the condition of cerebral ischemia and reperfusion. METHODS: Ninety-one male SD rats were randomly divided into 13 groups: sham operation group (S), model groups (group M6 h, group M24 h, group M72 h, group M7 d), apigenin treatment groups (group A6 h, group A24 h, group A72 h, group A7 d) and dexamethasone treatment groups (group D6 h, group D24 h, group D72 h, group D7 d). The acute transient focal cerebral ischemia reperfusion model was established by modified method of inserting the nylon thread into middle cerebral artery, staying for 2 h and then withdrawing from the artery. In the experiment groups, the TTC staining of brain slices were performed and the neurological behavior scores were determined. The expression of VEGF by immunohistochemistry (ICH) was semi-quantitatively analyzed by measuring the integrated absorbance(IA). RESULTS: Abnormal neurological behaviors were observed in the animals of M groups, A groups and D groups, but the neurological behaviors of the rats in A7 d group were better than that in the other groups (P<0.05). Typical cortical infarct lesions in M groups, A groups and D groups were found by TTC staining, mainly in cerebral cortex and striatum. The immunnohistochemical results showed that the expression of VEGF was significantly higher in M, A and D groups than that in S group (P<0.05). Moreover,the expression of VEGF in A groups(A24 h and A72 h)was higher than that in M groups (M 24 h and M72 h,respectively)(P<0.01).The expression of VEGF in D72 h group was higher than that in M72 h group (P<0.05), and that in A7 d group was obviously higher than that in D7 d group (P<0.01).CONCLUSION: Apigenin promotes the expression of VEGF in the model of acute transient focal cerebral ischemia-reperfusion injury, improves the process of brain injury and recovers the brain functions in rats. 相似文献
20.
AIM: To investigate the effets of naoluo xintong on the expression of Fas, FasL protein in hippocampus CA1 area and Fas mRNA in the cortex of frontal or parietal lobe after local cerebral ischemia/reperfusion in MCAO rats. METHODS: The local cerebral ischemia /reperfusion model was established by intraluminal thread occlusion of the middle cerebral arteries (MCAO), the middle cerebral arteries of rats were occluded for 2 hours and reperfused for 1, 3 and 7 days. The animals were divided into pseudo surgery group(sham group), model group, Yiqi group, Huoxue group and naoluo xintong group. Using the techniques of immuno-histochemical staining and in situ hybridization, the expression of Fas and FasL was observed in hippocampus CA1 area, the expression of Fas mRNA was also observed in the cortex of frontal and parietal lobe. RESULTS: A value of Fas and FasL protein expression or A value and positive unit of Fas mRNA expression in control group were higher than those in sham in hippocampus CA1 area, the cortex of frontal or parietal lobe after local cerebral ischemia/reperfusion in MCAO rats (P<0.01). A value and/or positive unit of their expression in naoluo xintong group were lower than those in control group (P<0.05 or P<0.01). A value and/or positive unit of their expression in Yiqi and Huoxue groups were higher than those in naoluo xintong group for 3 and/or 7 days (P<0.05 or P<0.01). CONCLUSION: naoluo xintong could resist neuron apoptosis, alleviate pathologic injury after local cerebral ischemia/reperfusion in MCAO rats by inhibiting the expression of Fas, FasL protein and Fas mRNA. 相似文献