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1.
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   

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To observe the effect of multiple electroacupuncture (EA) on the pain threshold and theregulation of N-methyl-D-aspartate (NMDA) receptor in dorsal root ganglia (DRG) of neuropathicpain rats. Rats were prepared with a unilateral chronic constriction injury (CCI) to the sciatic nerve.EA was done in acupoints "Huan Tiao" and "Yang Ling Quan" for 30 min every day and the thermalthresholds were detected after EA at 3, 5, 7, 10, 14 days after operation. On day 14 after nerve in-jury, the in situ hybridization method was used to investigate the change of NMDA R1 mRNA inL4—L5 DRG. The thermal threshold reduced significantly from day 3 after operation in CCI rats.After multiple EA treatment, the ipsilateral thermal hyperalgesia relieved gradually and the thermalthreshold had no difference with control side after day 5(P>0. 05). From Day 7 after operation, thethermal threshold at each time point were significantly different compared with CCI group respective-ly(P>0.05). Moreover the EA had accumulative effect.  相似文献   

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Objective:To explore the protective effects and mechanisms of electroacupuncture(EA)at Zusanli(ST36)acupoint in rats with severe acute pancreatitis(SAP).Methods:Sixty-six male SpragueDawley rats were randomly assigned to three groups of 22 each:a SAP model group(SAP group),a shamoperated group(sham group)and a EA at ST36 acupoint group(EA group).A rat model of SAP was induced by pancreatic duct injection with 3.5%sodium taurocholate.EA was performed at ST36 acupoint for 30 min after induction of SAP and 30 min before sacrificed.The rats were killed at 3 h(n=7),6 h(n=7)and 12 h(n=8)after operation,and blood samples were taken for the measurement of tumor necrosis factor-alpha(TNF-a),interleukin-6(IL-6)and acetylcholine(Ach)by enzyme-linked immunosorbnent assay.The pathological changes of pancreatic tissue,volume of ascites and pancreatic weight/body weight ratio were measured.Results:The serum concentrations of TNF-αand IL-6 in the EA group were significantly lower than in the SAP group at 3,6and 12 h after the operation(P0.05).Serum Ach in the EA group was significantly higher than in the SAP group at various time points after operation(P0.05).The other parameters were clearly improved after treatment with EA.Conclusion:EA at ST36 acupoint might have a therapeutic effect in rats with SAP through activating the cholinergic anti-inflammatory pathway.  相似文献   

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Objective To investigate the influence of acpuncture on free calcium in rat brain cells after focal cerebral ischemia reperfusion.Methods 145 adult male SD rats were randomly divided into control group,simple ischemia reperfusion group and acupuncture with ischemia reperfusion group.The middle cerebral artery occlusion/reperfusion (MCAO/R) rat model was established by the modified Longa occlusion method. ①The part of free calcium in rat brain cells,focal cevebral ischemia model of rats were made by thread locking up the blood vessel for 15 min.30 min later after reperfusion, the Baihui and Shuigou Point in Du meridian were acupunctured electrically 30 min.After 3h, 6h and 12h, the rat was killed and its brain cells were made into single cell suspension,marked by Fluo-3/AM.The fluorescence optical density was recorded by laser confocal microscopy.②The part of nerve functional reconstruction, focal cevebral ischemia model of rats were made by thread locking up the blood vessel for 12 hours.30 min later after reperfusion, the Baihui and Shuigou Point in Du meridian were acupunctured electrically 30 min.After 7 d, 14 d,30 d,60 d and 90 d, the rat was forced to detect it's strength of the dog.Results ①Free calcium in rats of acupuncture therapy group(6h:10.96±1.18;2h:20.9±4.37) was significantly less than that in control group in 6 h and 12 h after reperfusion (6 h: 16.87 ± 3.56,12 h: 34.10 ±1.06)(P<0.05).②The dog in rats of acupuncture therapy group was significantly more than that in control group in 7 d, 14 d after reperfusion (P< 0.05 ).No difference of the dog was detected in 30 d ,60 d and 90 d after reperfusion between the two groups.Conclusion Acupunture could decreases the concentration of free calcium and the expression of Caspase-3 mRNA in rat brain cells after focal cerebral ischemia reperfusion, and it can facilitate the recovery of nerve function.  相似文献   

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Objective To investigate the influence of acpuncture on free calcium in rat brain cells after focal cerebral ischemia reperfusion.Methods 145 adult male SD rats were randomly divided into control group,simple ischemia reperfusion group and acupuncture with ischemia reperfusion group.The middle cerebral artery occlusion/reperfusion (MCAO/R) rat model was established by the modified Longa occlusion method. ①The part of free calcium in rat brain cells,focal cevebral ischemia model of rats were made by thread locking up the blood vessel for 15 min.30 min later after reperfusion, the Baihui and Shuigou Point in Du meridian were acupunctured electrically 30 min.After 3h, 6h and 12h, the rat was killed and its brain cells were made into single cell suspension,marked by Fluo-3/AM.The fluorescence optical density was recorded by laser confocal microscopy.②The part of nerve functional reconstruction, focal cevebral ischemia model of rats were made by thread locking up the blood vessel for 12 hours.30 min later after reperfusion, the Baihui and Shuigou Point in Du meridian were acupunctured electrically 30 min.After 7 d, 14 d,30 d,60 d and 90 d, the rat was forced to detect it's strength of the dog.Results ①Free calcium in rats of acupuncture therapy group(6h:10.96±1.18;2h:20.9±4.37) was significantly less than that in control group in 6 h and 12 h after reperfusion (6 h: 16.87 ± 3.56,12 h: 34.10 ±1.06)(P<0.05).②The dog in rats of acupuncture therapy group was significantly more than that in control group in 7 d, 14 d after reperfusion (P< 0.05 ).No difference of the dog was detected in 30 d ,60 d and 90 d after reperfusion between the two groups.Conclusion Acupunture could decreases the concentration of free calcium and the expression of Caspase-3 mRNA in rat brain cells after focal cerebral ischemia reperfusion, and it can facilitate the recovery of nerve function.  相似文献   

7.
To examine the effect of Gankang Suppository on duck hepatitis B virus (DHBV), the serum biochemistry and hepatic histology in an animal model of DHBV infection, a model of DHBV infection was established by infecting 1-day-old Yingtaogu ducklings with DHBV-positive serum. The successful model was confirmed by PCR assay and 48 ducklings infected with DHBV were randomly divided into 3 groups: a Gankang Suppository treatment group, an acyclovir (ACV) group and a DHBV model group (control), with each group having 16 animals. All the animals were given the medicines for 4 weeks in a row. The serum of the animals was taken 14 and 28 days after the medica- tion and 7 days after drug discontinuation. Real-time PCR was performed to detect the copy numbers of DHBV DNA in the serum. ALT and AST were dynamically monitored. The ducklings were sacrificed on the 7th day after the discontinuation of the treatment and livers were harvested and examined for inflammation and degeneration of liver cells by using HE staining. The results showed that on day 14, 28 after the treatment and day 7 after the withdrawal, the logarithmic values (log) of DHBV DNA copy numbers in ducklings of Gankang Suppository treatment group were significantly lower than that before the treatment (P=0.0092, P=0.0070, P=0.0080, respectively). Compared with DHBV model control group, the ALT level was significantly decreased (P=0.0020, P=0.0019, respectively) on day 28 after the treatment and on day 7 after the withdrawal. The AST level was also reduced on day 14 after the treatment (P=0.0298). Compared with the ACV control group, the level of ALT was lower on day 7 after the withdrawal (P=0.0016). Histologically, the hepatocyte swelling, vacuolous degeneration and acidophilic degeneration in Gankang Suppository treatment group were alleviated 7 days after the withdrawal as compared with model control group (P=0.0282, P=0.0084, P=0.0195, respectively). It is concluded that Gankang Suppository can effectively suppress DHBV  相似文献   

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Background Preconditioning with repeated electroacupuncture (EA) could mimic ischemic preconditioning to induce cerebral ischemic tolerance in rats. The present study was designed to investigate whether mu(μ)-, delta(δ)- or kappa(κ)-opioid receptors are involved in the neuroprotecUon induced by repeated EA preconditioning. Methods The rats were pretreated with naltrindole (NTI), nor-binaltorphimine (nor-BNI) or D-Phe-Cys-Tyr-D- Trp-Om-Thr-Pen-Thr-NH2 (CTOP), which is a highly selective δ-, κ- or μ-opioid receptor antagonist respectively, before each EA preconditioning (30 minutes per day, 5 days). Twenty-four hours after the last EA treatment, the middle cerebral artery occlusion (MCAO) was induced for 120 minutes. The brain infarct volume was determined with 2,3,5-tdphenyltetrazolium chloride staining at 24 hours after MCAO and compared with that in rats which only received EA preconditioning. In another experiment, the met-enkephalin-like immunoreactivity in rat brain was investigated by immunohistochemistry in both EA preconditioning and control rats. Results The EA preconditioning reduced brain infarct volume compared with the control rats (P=-0.000). Administration of both NTI and CTOP attenuated the brain infarct volume reduction induced by EA preconditioning, presenting with larger infarct volume than that in the EA preconditioning rats (P〈0.001). But nor-BNI administration did not block the infarct volume reduction induced by EA preconditioning, presenting with smaller infarct volume than the control group rats (P=-0.000). The number of met-enkephalin-like immunoreactivity positive neurons in the EA preconditioning rats was more than that of the control rats (P=-0.000). Conclusion Repeated EA preconditioning stimulates the release of enkephalins, which may bind 5- and p-opioid receptors to induce the tolerance against focal cerebral ischemia.  相似文献   

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Objective: To investigate the effects of electroacupuncture and ischemic preconditioning (IPC) on circulatory function in pigs with myocardial ischemia/reperfusion injury. Method: Eighteen pigs with myocardial ischemia/reperfusion injury were randomly allocated into three groups, 6 in each. Group I was the control group, group II was the group that received IPC, and group III was that received both electroacupuncture and IPC. Blood malondialdehyde (MDA), superoxide dismutase (SOD), creatine phos-phokinase (CPK) and its isoenzyme (CK-MB), coronary artery flow and myocardial heat-shock protein (HSP) mRNA expression were detected for evaluation. Results: After treatment, the MDA content was decreased and SOD activities increased significantly in the acupuncture and IPC group compared with the control group (P<0. 05 respectively). The levels of CPK, CK-MB at 20, 60 min after reperfusion were significantly higher than those before treatment, but the levels in group III and group n were remarkably lower than  相似文献   

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Objective: To observe the effects of electroacupuncture on hippocampal and cortical apoptosis in a mouse model of cerebral ischemia-reperfusion injury. Methods: Mouse models established by repeated cerebral ischemia-reperfusion, followed by electroacupuncture at Shenshu, Geshu, and Baihui points. The control group mice were intragastrically administered Hydergine. On day 1 and 7 post-treatment, hippocampal and cortical apoptosis was detected by terminal-deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL), and apoptosis images in the hippocampal CA1 zone and cortical area were analyzed. Results: In the model group, apoptotic cells were detected one day after treatment and some cellular fibers were disarrayed. By day 7 post-treatment, there was an increase in the number of apoptotic cells in the hippocampal CA1 region. In addition, there were apoptotic cells in the cortical area, the cortical layers were thinner with localized neuronal loss and sieve-like lymphocyte infiltration, as well as glial cell proliferation and visible infarct lesions. However, in the Hydergine and electroacupuncture groups, there was a small number of apoptotic cells. At 7 days post-treatment in the model group, field number, numerical density on area, and surface density were increased. However, in the Hydergine and electroacupuncture groups these parameters were decreased (P<0.01), with a significant difference between the two treatment groups (P<0.01). Conclusion: Electroacupuncture treatment inhibited apoptosis and provided neuroprotection.  相似文献   

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目的 观察电针及电针结合脑内注射血管内皮生长因子(VEGF)对脑缺血后再灌注损伤大鼠caspase12、caspasse3、 葡萄糖调节蛋白-78 (GRP78)的影响,探讨电针结合脑内VEGF对脑缺血后再灌注损伤的修复机制。方法 将60只雄性SD大鼠随机分为假手术组、模型组、电针组、电针+VEGF组,每组15只。后3组采用线栓法进行大脑中动脉缺血(MCAO)法制作脑缺血后再灌注损伤模型。电针组及电针+VEGF组造模后1 d开始电针干预(穴位:百会、曲池、足三里),1次/d,每次30 min,共14 d。电针+VEGF组大鼠于造模成功后24 h行第一次电针干预后,向侧脑室内一次性注入10 μL VEGF165 (0.025 μg/μL)。每组于0 d(造模后1 d,开始电针干预前)、7 d、14 d时,各取5只大鼠进行神经功能评分(mNSS)后处死取材,尼氏染色观察脑梗死区组织形态,免疫组化法检测大鼠缺血脑组织GRP78活性,real-time PCR法检测大鼠缺血脑组织caspase12、caspase3、GRP78 mRNA表达量。结果 0 d、7 d、14 d时,与假手术组比较,模型组大鼠mNSS评分升高( P<0.05),镜下可见脑梗死征象(尼氏小体数量明显减少且排列混乱,结构不清晰),GRP78免疫阳性细胞数量增多,GRP78 mRNA表达升高( P<0.05),caspase12及caspase3 mRNA表达升高( P<0.05)。7 d和14 d时,与模型组比较,电针组以及电针+VEGF组大鼠的mNSS评分降低( P<0.05),镜下脑梗死征象减轻,GRP78免疫阳性细胞数量增多,GRP78 mRNA表达增多( P<0.05),caspase12、caspase3 mRNA表达降低( P<0.05),电针+VEGF组上述指标变化均较电针组明显( P<0.05)。假手术组各时点间上述指标差异无统计学意义( P>0.05),其余3组mNSS评分( P<0.05)、脑梗死征象、caspase12、caspase3 mRNA表达随治疗时间降低( P<0.05),GRP78免疫阳性细胞数量随治疗时间增多,GRP78 mRNA表达随治疗时间升高( P<0.05)。结论 电针结合脑内注射VEGF可促进脑缺血损伤组织修复,其机制可能与下调caspase12、caspase3基因,上调GRP78基因的表达有关,且其效果比单纯使用电针法更具优势。  相似文献   

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目的:研究异氟烷预处理局灶性脑缺血成年大鼠模型,通过检测缺氧诱导因子1α( HIF-1α)、血红素氧合酶1(HO-1)以及 B 细胞淋巴瘤因子2(Bcl-2)表达水平揭示其脑保护作用。方法2月龄 SD 大鼠随机分为假手术组、单纯大脑中动脉闭塞模型组(MCAO 组)、异氟烷预处理组(ISO组),缺血再灌注采用90 min 大脑中动脉闭塞 MCAO,MCAO之前 ISO 组进行30 min 异氟烷预处理,30 min 空气洗脱。再灌注24 h 检测神经功能评分及脑梗死面积,MCAO 建模后再灌注6、24、72 h 收集大鼠脑皮层组织,Western blot 法检测HIF-1α、HO-1以及 Bcl-2表达水平。结果 MCAO 组术后24 h 改良神经损伤严重程度评分(mNSS 评分)明显低于 ISO组(P <0.05)。再灌注24 h 检测结果显示,ISO 组神经损伤及脑梗死面积明显小于 MCAO 组(P <0.05)。建模6、24 h后 MCAO 组和 ISO 组 HIF-1α、HO-1以及 Bcl-2表达水平显著上升(P <0.05),24 h 达到峰值,72 h 时间点各指标与假手术组间差异无统计学意义(P >0.05)。结论 ISO 预处理通过上调 HIF-1α、HO-1以及 Bcl-2表达发挥脑保护作用,但非长效作用。  相似文献   

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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   

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目的 观察电针对大脑中动脉缺血大鼠缺血皮质区内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)及一氧化氮(nitric oxide,NO)的调控作用。方法 取SPF级健康雄性大鼠随机分为假手术组、模型组、电针组,每组14只,利用改良线栓法制备脑缺血大鼠模型,电针组选取“百会”“风府”“内关”“心俞”4个穴位,从第1天术后4 h开始治疗,每日1次,共治疗7 d。干预结束后,比较各组大鼠神经功能评分、脑梗死体积、脑缺血皮质区细胞病理表现、缺血皮质区eNOS蛋白的表达、血清NO的含量。结果 与假手术组比较,模型组大鼠神经功能缺损体征明显(P<0.05),梗死范围显著,脑缺血皮质区eNOS蛋白表达显著下降(P<0.05),血清NO含量升高(P<0.05);与模型组比较,电针组大鼠神经功能缺损评分降低(P<0.05),脑梗死体积明显缩小(P<0.05),脑皮质缺血区eNOS蛋白表达水平显著上升(P<0.05),血清NO含量升高(P<0.05)。结论 电针可促进局灶性脑缺血大鼠神经功能的恢复并缩小脑梗死体积,其机制可能与调控血管新生相关因子eNOS、NO表达增多有关。  相似文献   

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目的探讨电针刺激头部穴位对急性脑缺血再灌注损伤大鼠血清中转化生长因子-β1(TGF-β1)含量的影响。方法将72只健康SD雄性大鼠随机分为假手术组、模型组、电针组,分别为8、32、32只;再根据缺血再灌注12、24、48、72 h不同的时间点,电针组和模型组再随机分为4个亚组,每组8只。线栓法制备大脑中动脉闭塞再灌注模型。电针组选取头部百会穴、水沟穴,进针后将针柄分别连接至G6805-1型针灸治疗仪上,刺激参数:疏密波,频率2 Hz/150 Hz,强度3 mA,时间30 min;模型组和假手术组不予电针治疗。运用神经功能缺损评分(NSS)评价急性脑缺血再灌注12、24、48、72 h后各组大鼠神经功能缺损情况,酶联免疫吸附测定法检测急性脑缺血再灌注12、24、48、72 h大鼠血清中TGF-β1含量。结果模型组与电针组大鼠脑缺血再灌注12、24、48、72 h NSS和TGF-β1含量均较假手术组升高(P<0.05);与模型组比较,电针组各时相NSS均减低(P<0.05),TGF-β1含量均升高(P<0.05)。结论电针刺激能促进脑缺血再灌注损伤大鼠神经功能的修复,增加TGF-β1的含量,可能利于减缓脑缺血后的免疫炎症反应。  相似文献   

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目的观察电针预处理对大鼠脑缺血再灌注损伤后颈静脉血糖和脑组织含水量的影响。方法健康雄性Wister大鼠90只,随机分为假手术组(SH组,n=30只),脑缺血再灌注组(IR组,n=30只),电针预处理加脑缺血再灌注组(EA组,n=30只)。采用阻断双侧颈总动脉合并全身低血压方法建立大鼠全脑缺血模型,缺血15 min实施脑血流再灌注。电针预处理组在脑缺血开始前给予电针刺激穴位预处理30 min,穴位选择"百会"(Du20)与"水沟"(Du26)穴。在缺血再灌注后2、6、24 h,从颈静脉抽取血样测定血糖含量,然后断头取血,采用干-湿重法测定大鼠脑组织含水量。结果 IR组和SH组以及EA组的脑含水量在术后2 h无明显差别。与SH组比较,IR组和EA组脑含水量在再灌注后6 h明显升高(P〈0.01)。EA组在再灌注后6 h和24 h脑含水量显著低于IR组(P〈0.01)。和SH组比较,EA组和IR组在再灌注后2 h血糖明显升高,6 h达到高峰至24 h后有所回落(P〈0.01)。EA组在再灌注2 h,6 h和24 h血糖值显著低于IR组(P〈0.01)。结论电针预处理能够显著降低脑缺血灌注大鼠血糖上升水平,可以减轻脑缺血再灌注后脑水肿,从而减轻脑缺血再灌注损伤。  相似文献   

17.
 目的 研究电针干预大鼠脑缺血再灌注损伤时脑内水通道蛋白4 (aquaporin 4,AQP4)的表达与分布改变。 方法 选用SD雄性大鼠406只,分为正常对照组(n=40),脑缺血组(n=138),脑缺血+电针组(电针处理组,n=138)和脑缺血+假电针组(n=90)。利用线栓法制作大鼠大脑中动脉阻塞(middle cerebral artery occlusion,MCAO)模型,缺血1 h后实施脑血流再灌注。电针处理组在脑缺血开始后立即给予电针刺激,穴位选择“水沟”(GV 26)与“百会”(GV 20)。利用Western blot检测AQP4的蛋白表达水平,胶体金免疫电镜观察AQP4免疫阳性颗粒在血管周边的分布,常规焦油紫染色计算脑缺血后的脑梗死体积以及脑肿胀程度。神经行为学评估通过Garcia量表进行评分。结果 (1)再灌注24 h内,电针可下调因脑缺血而诱导的AQP4表达升高,再灌注后6 h和12 h分别是缺血组的0.63倍和0.72倍(P < 0.05);(2)与正常对照组相比,血管周边AQP4的免疫阳性颗粒在再灌注后6 h增多,在再灌注后24 h减少,电针干预组中血管周边AQP4的免疫阳性颗粒密度发生改变,其变化与缺血组相反,差异有统计学意义(P < 0.05);(3)电针减轻脑缺血后的脑梗死及脑肿胀,促进神经行为功能的恢复。结论 电针下调因缺血而导致的AQP4蛋白的表达升高,并动态改变其在血管周边的分布。电针对AQP4的调控作用可能与电针的神经保护作用机制相关。  相似文献   

18.
电针上调δ阿片受体的表达减轻大鼠急性缺血性脑损伤   总被引:1,自引:0,他引:1  
目的:探讨δ-阿片受体(delta—opioid receptor,DOR)在电针抗急性脑缺血损伤中的作用。方法:51只大鼠随机分为假手术组、假电针组、模型组、电针组、DOR拮抗剂+电针组。除假手术组外,其余各组均用大脑中动脉线栓法致大鼠局部脑缺血并行再灌注。电针干再灌注时开始.持续30min。再灌注24h后检查神经功能缺损程度、脑梗死体积。另取12只大鼠分为假手术组、模型组、电针组和DOR拮抗剂+电针组.蛋白印迹法检测脑组织中DOR蛋白的表达。结果:与模型组、假电针组比较,电针组脑梗死体积减小(P〈0.05),神经功能缺损评分增加(P〈0.05)。电针组60kD的DOR蛋白表达较模型组增加(P〈10.05),36kD的DOR蛋白表达有增加趋势,但差异无统计学意义。DOR拮抗剂+电针组脑梗死体积、神经功能缺损评分与模型组和假电针组比较,差异无统计学意义.DOR蛋白表达和模型组比较。差异亦无统计学意义。结论:电针通过增加DOR的表达减轻缺血性脑梗死和神经功能缺损。  相似文献   

19.
目的:比较督脉取穴法("人中"、"百会"穴)和背俞穴取穴法("肝俞"、"肾俞"穴)抗急性脑缺血损伤的效果.方法:成年健康雄性SD大鼠80只,采用线栓法造成右侧大脑中动脉阻断(Middle cerebral artery occlusion,MCAO)模型后,随机分为假手术组(n=5)、模型组(n=25)、电针人中+百会...  相似文献   

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