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1.
Local hypothermia and optimal temperature for stroke therapy in rats   总被引:2,自引:0,他引:2  
Background Local hypothermia induced by intravascular infusion of cold saline solution effectively reduces brain damage in stroke. We further determined the optimal temperature of local hypothermia in our study. Methods Seventy-eight adult male Sprague Dawley rats (260-300 g) were randomly divided into 3 groups: group A, ischemia/reperfusion without cold saline infusion (n=26) (control group); group B, infusion with 20℃ saline before reperfusion (n=26); group C: infusion with 10℃ saline before reperfusion (n=26). In each group, we chose 15 rats for monitoring physical indexes and the temperature of the brain (cortex and striatum) and body (anus), measurement of brain infarction volume, assessment of neurological deficits and the survival rate of reperfusion at 48 hours. Another 8 rats from each group was chosen for examining brain edema, another 3 from each group for histological observation by electron microscopy (EM) and light microscopy (LM) at 48 hours after reperfusion. Results There was no significant difference among the 3 groups for physical indexes during the examination (F(2. 45)= 0.577, P=0.568; F(2.45)= 0.42, P=0.78 for blood pressure and blood gas analysis, respectively). The brain temperature was significantly reduced in the group C compared to the other groups (F(2.45)=37.074, P=0.000; F(2.45)=32.983, P=0.000, for cortex and striatum temperature respectively), while the difference in rectal temperature between group A and B or C after reperfusion was not significant (F(2.45)= 0.17115,P=0.637). And the brain infarct volume was significantly reduced in group C (from 40%±10% in group A, 26%±8% in group B, to 12%±6% in group C, F(2.45)=43.465, P=0.000) with the neurological deficits improving in group C (Х^2=27.626, P=0.000). The survival rate at 48 hours after 10℃ and 20℃ saline reperfusion was increased by 132.5% and 150%, respectively, as compared to the control group (Х^2=10.489, P=0.005). The extent of the brain edema showed no significant difference (F(2.21)=0.547, P=0.587) after cold saline infusion compared to the control group. No obvious vascular injury was found by electron or light microscopy in either infusion group. Conclusions Regional hypothermia with 10℃ cold saline infusion can significantly decrease the infarction volume, improve the neurological deficits, and 10℃ seems to be the optimal temperature in inducing a cerebral protection effect during stroke. This procedure could be adopted as a further treatment for acute stroke patients.  相似文献   

2.
The change of the expression of Cyclins in neurons of rats after focal cerebral ischemia was investigated. Ischemia was induced by temporary middle cerebral artery occlusion (MCAO). The experimental rats induced by MCAO were sacrificed on 7th and 14th day after reperfusion. The brain was taken out at 7th and 14th day after injury, and the expression of Cyclin D1, E, A and B1 in neurons of cerebral cortex or hippocampal CA1 region was detected by immunofluorescence and confocal microscope. The results showed that after MCAO, in the ipsilateral CA1 subfield of hippocampus the expression of Cyclin D1, E, A and B1 in neurons was significantly gradually up-regulated at 7th and 14th day after reperfusion (P〈0.05) as compared with that in control group. In the ipsilateral cerebral cortex the expression of Cyclin D1 and B1 in neurons was notably gradually down-regulated at 7th and 14th day, and that of Cyclin E and A was significantly up-regulated at 14th day after reperfusion as compared with that in control group (all P〈0.05). It was concluded that there was a differential sensitivity among neurons from different brain regions to ischemic injury. But all of them re-enter into cell cycle after MCAO.  相似文献   

3.
Objective:To investigate the effect of Buyang Huanwu Decoction(补阳还五汤,BYHWD) on estradiol(E2) and estradiol receptor(ER) in serum and brain in ovariectomized rats after middle cerebral artery occlusion(MCAO).Methods:Adult female rats were ovariectomized and focal cerebral ischemic was induced by MCAO.Rats were randomly divided into normal,ovariectomy(OVX),MCAO,OVX+MCAO,OVX+MCAO+E2,and OVX+MCAO+BYHWD group.Rats were administered BYHWD 5 g/kg daily,estradiol valerate 500 μg/kg per day or distilled water for 7 consecutive days.Neuronal function and infarct volume were measured on day 7 after artery occlusion,and E2 and ER concentration in serum and brain were checked by enzyme-linked immunosorbent assay.Results:BYHWD significantly improved the neurological behavior,reduced the infarction volume,increased E2concentration in serum and brain,and increased ER concentration in the brain in ovariectomized rats after MCAO.Conclusion:The neuroprotective effects of BYHWD are associated with estrogen and its receptor.  相似文献   

4.
Objective: To observe the effect of electroacupuncture (EA) on expression of p53 protein in cerebral cortex of senile rats with global cerebral ischemia/reperfusion (IR) injury and to explore its mechanism. Methods: The cerebral IR injury rat model was established referring to Pulsinelli 4-vessel occlusion method. Thirty-six SD rats were randomly and evenly divided into the control group, the IR group and the IR plus EA (IR-EA) group. The animals in the control group were subjected to electrocauterization of vertebral arteries in bilateral flank orifice alone with the general carotid arteries unoccluded. To rats in the IR-EA group, immediately and 24h, 48h, 72h after cerebral IR, EA treatment on bilateral acupoint "Zusanli" (ST36) was applied once a day, lasting for 60 minutes. After the final treatment, all the rats were sacrificed and their brains were taken to examine p53 protein expression by the immunohistochemical method. Results: Cells with positive p53 immunoreactivity in the cerebral cortex of  相似文献   

5.
Objective To investigate whether pretreatment with repeated electroacupuncture (EA)at th e Baihui acupoint could induce ischemic tolerance against transient focal cerebr al ischemic injury in rats. Methods Thirty male Sprague- Dawley (SD) rats were randomly divided into 3 groups (n=10 for each): the control group consisted of animals receiving no treatment, the is oflurane (ISO) group had animals that inhaled 1.5% isoflurane for 30 min a day for 5 days, and animals in the EA group received electroacupuncture at the Baihu i acupoint for 30 min a day for 5 days under 1.5% isoflurane anesthesia. Twent y- four hours after the last treatment, the middle cerebral artery was occluded with No. 3 nylon monofilament for 120 min. The neurological outcomes were evalu ated 24 h after reperfusion. The infarct volumes were then assessed using 2% tr iphenyltetrazolium chloride staining after the neurological outcome evaluation. Results The neurological deficit score (NDS) of the EA group [1 (0-2)] was lower tha n that of the ISO group [2 (1-3)] and the control group [2 (1-4)], P<0. 05. The infarct volume of the EA group (38.3±25.4 mm(3)) was significantly smaller than that of the control group (220.5±66.0 mm(3)) and the ISO group (168.6±57.6 mm(3)) 24 h after reperfusion. Conclusion Electroacupuncture at the Baihui acupoint 30 min a day for 5 days significantly reduces neurological injury induced by transient middle cerebral artery occlusion.  相似文献   

6.
Objective:To investigate the effect of HHI-Ⅰ(活血化瘀注射液Ⅰ号) on the cerebral microcirculation,the blood-brain barrier permeability in rats and anti-hypoxic activity in mice.Methods:(1) The blood microcirculation of the brain in rats was investigated by laser Doppler flowmetry with the probes laid on the cerebral pia mater or inserted into the brain parenchyma.(2) The protective action of HHI-Ⅰagainst the brain microcirculation disturbance induced by intravenous injection of high-molecular dextran(10%,9 mL/kg)...  相似文献   

7.
Objective To investigate the expression of cytochrome C in perihematomal brain tissue and its relationship with the histopathological change and formation of cerebral edema in patients with hypertensive cerebral hemorrhage.Methods Thirty four patients(23 male,11 female) of hypertensive cerebral hemorrhage in hospital from Sep.2001 to Sep.2002 were selected with a mean age 55.6± 10.2 years(from 35 to 75 years).The mean volume of hemorrhagic blood was 50.4±11.6 ml(from 25 to 85 ml).The perihematomal brain tissue was obtained from the minimally invasive surgery.Histopathological change and expressions of cytochrome C in perihematomal brain tissue was detected by histopathological and immunohistochemical techniques.The volume of perihematomal cerebral edema was determined by computed tomographic scan before operation.The results of staining and the volume of perihematomal cerebral edema were analyzed with double blind fashion.Results Perihematomal cerebral edema were found 12-72h after cerebral hemorrhage.Myelin sheath degeneration,condensation of nucleus and typical apopototic body were observed in perihematomal brain tissue.Expression of cytochrome C in perihematomal brain tissue was observed at 4 h and reached peak around 48-72 h after cerebral hemorrhage.Cytochrome C expressed higher positively in 16 patients and lower positively in 13 patients.Cytochrome C expression was not detected only in 5 patints.There were significant differences in volume of perihematomal cerebral edema with different expression of cytochrome C in perihematomal brain tissue(P<0.01).Conclusions Cytochrome C expression was upregulated in perihematomal brain tissue in patients with hypertensive cerebral hemorrhage.Cytochrome C might involve in the histopathological change and the formation of perihematomal cerebral edema  相似文献   

8.
Objective: To observe and elucidate the neuroprotective effect of Xingnaojing (XNJ) injection on hippocampal N-methyl-D-aspartic acid (NMDA) receptors of focal cerebral ischemia in rats. Methods: Cerebral ischemia was established by occluding the middle cerebral artery with an intraluminal suture technique in rats. Neurological deficit score, infarct volume and quantity of NMDA receptors were estimated in all groups and compared. Results: After being treated with XNJ, the score decreased in the initial 6 hours and infarct volume decreased in 24 hours. And within 24 hours, the quantity of NMDA receptors obviously decreased compared with the model group (P<0. 01) It indicated that XNJ could ameliorate neurological behavior of middle cerebral artery occlusion rats and down-regulate the expression of hippocampal NMDA receptors. Conclusion: The neuroprotective effect of XNJ on focal cerebral ischemia is possibly related to down-regulating the expression of NMDA receptors in rats.  相似文献   

9.
Objective:To explore the protective effect of sound preconditioning against ototoxicity induced by cisplatin and its possible mechanism with respect to the nitric oxide (NO) pathway. Methods: Albino guinea pigs were divided into silent control, CDDP,sound preconditioning and sound preconditioning+CDDP groups. The animals of the CDDP group were injected with cisplatin intravenously 8 mg/kg b.w. The animals in the sound preconditioning were exposed to white noise at 85dB SPL, 5h/d, for 10 d (sound preconditioning). The animals in the sound preconditioning+CDDP group were treated with sound preconditioning first and then administrated with cisplatin intravenously 8 mg/kg b.w. Hearing thresholds of auditory brainstem responses (ABRs) of all animals were measured to evaluate hearing function. Hair cell loss was estimated via surface preparation. Cochlear tissue was assayed for measurement of NO level and immunohistochemistry method was used for inducible nitric oxide synthase (iNOS) analysis. Results: There was no significant difference between the silent control and sound preconditioning animals with respect to either functional or histological measures. Among the animals in the CDDP group, there was a significant elevation of threshold at the high test frequencies after administration compared with the silent control group (P〈0. 05). Morphological examination showed that there was obvious loss of the OHC, especially in the third row of the basal turn. The NO level and immunoreactivity to iNOS in this group were higher and more intensive than those of the silent control group (P〈0. 05). The ABR thresholds in the sound preconditioning + CDDP group were much lower than those of the CDDP group (P〈0.05). Slight sporadic loss of OHC was found in this group. The immunoreactivity to iNOS and the level of NO in cochlea decreased significantly compared with the CDDP group (P〈 0. 05). Conclusion: It is suggested that sound preconditioning, to some extent, provides protective effect against ototoxicity of cisplatin. The excess synthesis of NO induced by the over-expressed of iNOS may be involved in the CDDP induced ototoxicity. The possible mechanism is related to suppression of the NO pathway.  相似文献   

10.
Objective:To investigate the effect of electro-acupuncture(EA)on vasomotor symptoms in rats with acute cerebral infarction,by observing the changes in the expression of factors related to the phosphatidylinositol(PI)system.Methods:Forty-two Wistar rats were randomly divided into 3 groups by a random number table:the control group(n=6),the model group(n=18)and the EA group(n=18).The EA group was given EA treatment at Shuigou(GV 26)instantly after modeling with middle cerebral artery occlusion(MCAO)method,while the model and control groups were not given any treatment.The degrees of neurological deficiency were evaluated using neurological severity scores(NSS)and the brain blood flow was evaluated by a laser scanning confocal microscope.Western blot analysis was conducted to detect the expression levels of G-protein subtype(Gq)and calmodulin(CaM).Competition for protein binding was conducted to detect the expression level of inositol triphosphate(IP3).Thin layer quantitative analysis was conducted to detect the expression level of diacylglycerol(DAG).The expression level of intracellular concentration of free calcium ion([Ca2+]i)was detected by flow cytometry.Results:The NSS of the model group was significantly higher than the control group at 3 and 6 h after MCAO(P<0.01),while the EA group was significantly lower than the model group at 6 h(P<0.01).The cerebral blood flow in the model group was significantly lower than the control group at 1,3 and 6 h after MCAO(P<0.01),while for the EA group it was remarkably higher than the model group at the same time points(P<0.01).The expressions of Gq,CaM,IP3,DAG and[Ca2+]i in the model group were significantly higher than the control group(P<0.05 or P<0.01),and those in the EA group were significantly lower than the model group at the same time points(P<0.05 or P<0.01).Conclusion:EA treatment at GV 26 can effectively decrease the over-expression of related factors of PI system in rats with acute cerebral infarction,improve cerebral autonomy movement,and alleviate cerebral vascular spasm.  相似文献   

11.
Objective: To investigate the potential mechanisms of electroacupuncture (EA) to prevent ischemic stroke. Methods: The method of middle cerebral artery occlusion (MCAO) was employed to establish a rat model of ischemic stroke. Seventy-eight Sprague-Dawley rats were divided into the sham group, MCAO + EA control (EC) group, and MCAO + EA (EA) group according to a random number table (n=26 per group). EA was applied to the acupoints of Baihui (DU 20) and Shenting (DU 24) 5 min and 6 h, respectively after the onset of MCAO for 30 min. Rats in the sham and EC groups received only light isoflurane anesthesia for 30 min after MCAO. The neuroprotective effects of EA were evaluated by rota-rod test, neurological deficit scores and infarct volumes. Additionally, Nissl staining and immunostaining were performed to examine brain damage, rod formation, cellular apoptosis, and neuronal loss induced by ischemia. The activities of caspase-3, and expression levels of cofilin and p-cofilin in mitochondria and cytoplasm after ischemic injury were determined by Western blot. Results: Compared with the EC group, EA significantly improved neuromotor function and cognitive ability after ischemic stroke (P<0.05 or P<0.01). Therapeutic use of EA also resulted in a significant decrease of cofilin rod formation and microtubule-associated protein-2 (MAP2) degradation in the cortical penumbra area compared with the EC rats (P<0.01). Furthermore, Western blot analysis showed that EA stimulation significantly inhibited mitochondrial translocation of cofilin and caspase-3 cleavage (P<0.05 or P<0.01). Additionally, brain damage (infarct volume and neuropathy), cellular apoptosis and neuronal loss induced by ischemia were remarkably suppressed by EA in the cortical penumbra of rats (P<0.05 or P<0.01). Conclusion: EA treatment after ischemic stroke may attenuate ischemic brain injury and cellular apoptosis through the regulation of mitochondrial translocation of cofilin, a novel mechanism of EA therapy.  相似文献   

12.
吸氧预处理对大鼠局灶性脑缺血损伤的保护作用   总被引:1,自引:0,他引:1  
张西京  熊利泽  胡文能  郑玉  路志红 《医学争鸣》2002,23(15):1349-1352
目的 研究吸入不同时间 10 0 % O2 能否诱导脑缺血耐受而对脑缺血再灌注损伤产生保护作用 .方法  6 3只 SD大鼠随机分为 7组 (每组 n=9) :即 A组 (对照组 )于缺血前 2 4h吸空气 2 4 h;B,C和 D组分别于缺血前 2 4 h连续吸 10 0 %O2 2 4 ,12和 6 h;E,F和 G组分别连续吸 10 0 % O2 2 4 ,12和 6 h. A,B,C和 D组于吸氧结束后 2 4 h造成脑缺血 ;E组于吸氧后即刻造成脑缺血模型 ;F组间隔 12 h;G组间隔 18h后造成脑缺血 .局灶性脑缺血模型采用 3- 0尼龙线线栓法栓塞大脑中动脉 ,2 h后拔出尼龙线使血液再灌注 .脑缺血 2 h和再灌注后 2 4 h行脑功能障碍评分 ,并处死动物取大脑行TTC染色测量脑梗死容积 .结果  B组的脑功能障碍评分与A组相比显著降低 (P<0 .0 5 ) ,C,D,E,F和 G组与 A组相比无显著性差异 ;脑梗死容积 B组 (10 4 .8± 6 2 .1) mm3显著小于 A组 (199.0± 6 9.6 ) mm3(P<0 .0 1) .吸 10 0 % O2 12 h及6 h组及吸 10 0 % O2 2 4 h后即刻造成脑缺血组与对照组相比其脑梗死容积无明显差异 .结论 本实验首次证实连续吸10 0 % O2 2 4 h且间隔一定时间后能模拟缺血预处理对大鼠短暂性脑缺血产生保护作用 .  相似文献   

13.
大鼠局灶性缺血预处理诱导的脑缺血耐受研究   总被引:1,自引:0,他引:1  
目的 观察局灶性缺血预处理所诱导的脑缺血耐受现象及其存在的时间窗。方法  86只 SD大鼠随机分为 PC、PC+ MCAO及 SS+ MCAO三组 ,分别给予 10 min大脑中动脉缺血预处理 ( PC)、PC+ 2 h大脑中动脉阻塞 ( MCAO)及假手术 ( SS) + 2 h MCAO,其中后两组又据 PC与 MCAO间隔不同分为 1d,3 d,7d,14d,2 1d,2 8d 6个亚组 ,MCAO后 2 4h处死 ,比较各组神经功能评分、梗死体积、含水量及组织病理变化。结果 单纯 PC不引起神经功能缺损及梗死形成 ;MCAO前 1~ 2 8d给予 PC组神经功能缺损均轻于 SS组 ( P<0 .0 1) ,其中 3 d组最明显 ;MCAO前 1~ 14d给予 PC者较 SS组梗死体积缩小 ( P<0 .0 5 ) ,尤以 3 d及 7d组明显 ,分别减小 5 3 .7%和49.9% ( P<0 .0 1) ;MCAO前 3 d给予 PC组脑含水量低于 SS组 ( P<0 .0 5 )。结论  10 min大脑中动脉预缺血不会引起神经损害但已足以诱导缺血耐受的产生 ;缺血耐受作用出现于 PC后 1d,其后 14d内给予 MCAO均可使梗死体积减小 ,而对神经功能的保护作用持续时间更长 ,至少可达 4周  相似文献   

14.
目的 探讨大麻素(CB)受体激动剂WIN 55,212-2预处理对大鼠局灶性脑缺血的保护作用.方法采用大鼠大脑中动脉栓塞(MCAO)致局灶性脑缺血模型,将50只雄性SD大鼠随机分为5组:对照组(Con组),行线栓法敛大脑中动脉栓塞(MCAO)前24 h腹腔注射生理盐水(NS)0.3ml;WIN 55,212-2预处理组(WIN1~3),分别于MCAO前24 h腹腔注射WIN 55,212-2 0.3,1和3rag/kg;DMSO组,于MCAO前24 h腹腔注射二甲基亚砜(DMSO,WIN 55,212-2的溶剂)0.3 ml.观察MCAO120 min再灌注24,48和72 h后神经功能评分(NFS)和再灌注72 h脑梗死容积百分比.结果 WIN 55,212-2预处理组大鼠NFS明显高于DMSO组和Con组(P<0.05),脑梗死容积百分比明显小于DMSO组和Con组(P<0.05).WIN2组和WIN3组的脑梗死容积百分比明显小于WIN1组,NFS明显高于WIN1组(P<0.05),WIN2组和WIN3组的NFS和脑梗死容积百分比差异无统计学意义(P=0.928),但3 mg/kg WIN 55,212-2可引起大鼠明显嗜睡和倦怠.结论 CB受体激动剂WIN 55,212-2预处理能诱导脑缺血耐受,对大鼠局灶性脑缺血再灌注损伤具有保护作用,并具有一定的剂量相火性.  相似文献   

15.
短暂地氟醚预处理对大鼠局灶性脑缺血损伤的保护作用   总被引:2,自引:0,他引:2  
目的:探讨短暂地氟醚预处理诱导脑缺血耐受的可行性。方法:30只雄性SD大鼠,随机分为三组:对照组动物不接受任何处理;吸氧组动物接受1 h吸氧预处理( 94%氧) ;地氟醚组动物吸入1 h5 .7%的地氟醚预处理。所有动物均采用右侧颈动脉尼龙线栓塞大脑中动脉致局灶性脑缺血1 2 0 min,观察再灌注后2 4 h神经行为学改变及脑梗死容积。结果:直肠温度、p H、PO2 、PCO2 、血压及血糖在预处理期间各组无明显差异。再灌后2 4 h神经行为学评分地氟醚组明显小于吸氧组和对照组( P<0 .0 5 ) ;地氟醚组脑梗死容积明显低于吸氧组和对照组,后两组梗死容积无显著性差异( P>0 .0 5 )。结论:短暂地氟醚预处理可通过诱导短暂局灶性脑缺血耐受而产生脑保护作用  相似文献   

16.
目的 研究短暂局灶性脑缺血预处理对再次脑缺血后微血管损伤及脑水肿的保护作用。方法 采用开颅方法阻断大鼠大脑中动脉(MCA)20min,3天后再次阻断24h。应用TTC染色、TUNEL及透射电镜技术,观察大鼠脑缺血后梗死灶体积、损伤侧服体积,组织病理学及超微结构改变。结果 同对照组相比,缺血预处理20min不引起明显的神经元损伤,而能使再次的24h局灶性脑缺血后梗死体积明显减小,微血管损伤及脑水肿明显减轻,半影区血管内皮细胞凋亡减少。结论 20min局生脑缺血预处理能够通过减轻微血管损伤及脑水肿对再次严重的脑缺血产生保护作用。  相似文献   

17.
目的:研究远隔缺血预适应( remote ischemic preconditioning,RIPC)对大鼠脑缺血再灌注后诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)表达的影响,以探讨 RIPC 保护脑缺血损伤的相关机制。方法应用线栓法制作大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型,将21只健康雄性 SD 大鼠采用数字表法随机分为3组:假手术组(sham,n=7),MCAO 组(n=7),RIPC+MCAO 组(n =7)。在 MCAO 手术前连续3 d,进行远隔肢体缺血预适应处理(双侧股动脉夹闭10 min/放开10 min,每天3次)。在缺血2 h-再灌注24 h 后进行神经功能评分,TTC 染色检测脑梗死体积,采用 Western blotting 方法检测梗死侧脑组织的 iNOS 蛋白表达水平。结果1)在 MCAO 手术过程中,3组实验动物的生理指标均在正常范围内,且组间差异无统计学意义。与 sham 组相比,MCAO 组大鼠再灌注24 h 时神经功能缺损评分显著升高、脑梗死体积明显增大(P〈0.05)。而 RIPC+MCAO 组大鼠神经功能较 MCAO 组大鼠得到明显改善、脑梗死体积显著减少(P〈0.05)。2)再灌注24 h 时,与 sham 组相比,MCAO 组大鼠脑梗死侧 iNOS 蛋白表达显著增加(P〈0.05)。与 MCAO 组相比,RIPC+MCAO 组大鼠脑梗死侧 iNOS 蛋白表达显著降低(P〈0.05)。结论 RIPC 处理对大鼠脑缺血损伤具有保护作用,其机制与降低脑缺血大鼠脑内 iNOS 蛋白表达有关。  相似文献   

18.
In 1990 ,Kitagawaetal1 firstfoundthatneuronalcellsinthegerbilhippocampuscoulddevelopresistancetoischemicneuronaldamageafterabriefperiodofreversibleischemia Thisphenomenon ,called“ischemictolerance” ,hasdrawnattentionbecausetheunderstandingofitsmechanismwil…  相似文献   

19.
目的 比较单独或联合应用人参皂甙Rd及远程预处理的脑保护效应,探寻安全有效的脑保护方法.方法 40只雄性SD大鼠随机均分为4组(n=10/组):①对照组(C组),腹腔注射生理盐水1 h后制备大脑中动脉栓塞-再灌注(middle cerebral artery occlusion-reperfusion,MCAO)模型;...  相似文献   

20.
目的研究R(+)-普拉克索[ R(+)-PPX]对短暂性局灶性脑缺血大鼠脑内活性氧自由基( reactive oxygen species,ROS)产生以及脑损伤的影响,探讨R(+)-PPX对脑缺血损伤的保护作用,寻找防治缺血性脑血管病的有效方法。方法采用数字表法随机将30只健康雄性SD大鼠分为:假手术组(Sham组,n=10);大脑中动脉梗死组(MCAO组,n=10);MCAO+R(+)-PPX组[于MCAO前30 min一次性腹腔注射R(+)-PPX,剂量为1 mg/kg,n=10]。使用线栓法制作大鼠缺血90 min再灌注模型,术中监测大鼠心率、平均动脉压及肛温,使其保持在正常范围。每组分别于脑缺血再灌注后6、24 h取脑组织行TTC染色检测大鼠脑梗死体积,并制作脑组织冰冻切片,采用H2DCF-DA染色法计数半暗带区ROS阳性细胞数目并检测其平均荧光强度。结果1)在MCAO手术过程中,Sham组、MCAO组和MCAO+R(+)-PPX组大鼠的心率、平均动脉压及肛温差异均无统计学意义。2)Sham组大鼠无脑梗死发生。缺血再灌注6 h及24 h,MCAO组、MCAO+R(+)-PPX组大鼠脑梗死体积均比Sham组显著增加(P〈0.05)且随再灌注时间延长递增(P〈0.05)。再灌注6 h时,MCAO+R(+)-PPX组与MCAO组相比,脑梗死体积明显减少,差异有统计学意义(P〈0.05),而再灌注24 h时,MCAO+R(+)-PPX组脑梗死体积与MCAO组相比差异无统计学意义(P 〉0.05)。3)Sham组大鼠脑内无缺血半暗带区。缺血再灌注6 h及24 h,MCAO组、MCAO+R(+)-PPX组大鼠脑缺血半暗带区域H2DCF-DA阳性染色细胞数目及平均荧光强度均随再灌注时间延长递增(P〈0.05)。再灌注6 h时,与MCAO组相比,MCAO+R(+)-PPX组的H2DCF-DA阳性染色细胞数目及平均荧光强度明显减少,差异有统计学意义(P〈0.05)。而再灌注24 h时,MCAO+R(+)-PPX组大鼠H2DCF-DA阳性染色细胞数目及平均荧光强度与MCAO组相比差异无统计学意义(P〉0.05?  相似文献   

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