电针对缺血性脑卒中大鼠记忆功能及脑内突触囊泡蛋白的影响

观察电针对缺血性脑卒中大鼠记忆功能及脑内突触囊泡蛋白（synaptic vesicular protein，SYN）的影响，探讨其可能的作用机制。方法 选取90 只SD大鼠随机分为模型组、电针组、假手术组，每组各30只。线拴法制作急性大脑中动脉缺血大鼠模型。电针组取“百会”“水沟”“内关”“三阴交”穴位，应用“醒脑开窍”法进行电针，每天电针30 min，连续电针6 d休1 d，7 d为一个疗程，首次电针干预在造模成功24 h后进行。模型组和假手术组不进行电针干预。大鼠分别按7、14、21 d 3个亚组进行运动及记忆功能评分，TTC染色测定脑梗死体积、Western blot检测脑内SYN的蛋白表达。结果 电针组运动功能评分较模型组显著降低（P<0.01），电针组进入隐藏区潜伏期时间较模型组显著缩短（P<0.01），电针组脑梗死率较模型组显著缩小（P<0.01），SYN的蛋白表达电针组较模型组明显增强（P<0.01）。假手术组无神经功能缺损及脑梗死灶，SYN表达最弱。结论 电针干预能减小脑梗死体积，上调脑内SYN的表达，进而促进缺血性脑卒中大鼠的记忆及运动等神经功能的恢复。     

Electroacupuncture Attenuates Surgical Stress-Induced Reduction of T Lymphocytes through Modulation of Peripheral Opioid System

Objective:To investigate the action mechanisms of electroacupuncture(EA)on postoperative immunosuppression.Methods:Male C57 BL/6 mice(5–7 weeks old)were randomly divided into:the sham injury group,the surgical trauma stressed group,the EA group[surgery+2/100 Hz EA at Neiguan(PC 6)],and the EA+Nal(surgery+EA+intraperitoneal injection of naloxone).Abdominal surgical trauma stress mice model was established.EA was performed on bilateral PC 6 acupoints by an EA apparatus(2/100 Hz)for 20 min once a day for 3 days.The m RNA expressions of MOR,DOR,and KOR in thymus and L3-5 dorsal root ganglions(DRG)were determined by quantitative real-time polymerase chain reaction(q RT-PCR)and the protein expressions of MOR,DOR,and KOR in thymus were measured by Western blot.Flow cytometry assay was used to detect the levels of T lymphocyte subtypes in the peripheral blood.Results:Surgical trauma induced decreased the m RNA expression level of MOR in both thymus(P<0.01)and L3-L5 DRGs(P<0.05).Moreover,EA treatment not only significantly attenuated the MOR protein and m RNA expression in the thymus(both P<0.05),but also markedly increased expression of DOR and KOR opioid receptor in thymus(P<0.01).However,the m RNA expressions of opioid receptors were not regulated by EA in the DRG(all P>0.05).Furthermore,T lymphocyte population of CD3^+ and CD4^+ was decreased in the peripheral blood after surgical trauma(both P<0.01).EA treatment can significantly elevate the population of CD3^+(P<0.01),CD4^+(P<0.05)and CD8^+T cells(P<0.01).Intraperitoneal injection of the non-selective opioid receptor antagonist naloxone blocked the up-regulation of T lymphocytes by EA.Conclusion:EA may improve postoperative immunosuppression through the peripheral opioid system.     

缺血性脑卒中的中医药治疗研究进展

缺血性脑卒中属于中医缺血性＂中风＂的范畴,具有发病率高、致残率高、预后差、易复发等特点。中医药治疗缺血性中风颇具优势,积累了丰富的理论知识和治疗经验。现就近年来中医药治疗缺血性脑卒中研究进展综述如下。     

缺血预适应对心肌缺血／再灌注损伤中细胞凋亡的作用

目的：探讨心肌缺血/再灌注损伤早期细胞凋亡的分布情况及缺血预适应的心肌保护作用是否与减少缺血区凋亡的发生有关。方法：将新西兰兔制成急性心肌缺血/再灌注损伤动物模型，随机分为两组：IR组和IP组。分区取心肌组织标本进行梗死面积大小及凋亡指数的检测。结果：IP组的梗死面积大小及凋亡指数均明显低于IR组。结论：心肌缺血/再灌注损伤早期细胞凋亡主要发生在缺血区的心肌组织中，缺血预适应可明显减少其发生。     

Changes of Apoptosis in Rats of Acute Ischemic Renal Injury under Treatment of Tetrandrine

Objective To elucidate the effect of tetrandrine on acute ischemic renal injury and its relation with apoptosis.Methods A model for bilateral post-ischemic renal injury in rats was developed by clamping renal pedicles for 45 min.Renal tissular DNA fragmentation analysis and renal tissular HE staining were used.Also quantitative analysis of apoptosis in injured renal tubular epithelium was carried out by using TdT-mediated dUTP nick and labeling(TUNEL).Results Apoptosis of renal tubular epithelium increased in acute ischemic renal injury.Tetrandrine could remarkably decrease the level of apoptosis in injured renal tubule while protecting renal tissue against the ischemic injuries.Conclusion Tetrandrine could adjust the level of apoptosis in renal tubular epithelium and alleviate renal tissular injury.     

中西医结合治疗缺血性脑卒中的成本效益分析

Objective:To evaluate the cost-effectiveness of combining Chinese medicine(CM)with Western medicine(WM)for ischemic stroke patients.Methods:Hospitalization summary reports between 2006 and 2010from eight hospitals in Beijing were used to analyze the length of stay(LOS),cost per stay(CPS),and outcomes at discharge.Results:Among 12,009 patients(female,36.44%;mean age,69.98±13.06 years old),a substantial number of patients were treated by the WM_Chinese patent medicine(CPM)_Chinese herbal medicine(CHM)(38.90%);followed by the WM_CPM(32.55%),the WM(24.26%),and the WM_CHM(4.15%).With adjustment for confounding variables,LOS of the WM_CPM_CHM group was about 10 days longer than that of the WM group,and about 6 days longer than that of the WM_CPM group or the WM_CHM group(P0.01);CPS of the WM_CPM_CHM group was United States dollar(USD)1,288 more than that of the WM group,and about USD600 more than that of the WM_CPM group or the WM_CHM group(P0.01).Compared with the WM group,odd ratio(OR)of recovered and improved outcome of the WM_CPM_CHM group was the highest[OR:12.76,95%confidence intervals(CI):9.23,17.64,P0.01],OR of death outcome of the WM_CPM_CHM group was the lowest(OR:0.08,95%CI:0.05,0.12,P0.01).There was no significant difference between LOS,CPS and OR of the WM_CPM group and those of the WM_CHM group(P0.05).Cost/effectiveness and incremental costeffectiveness ratio of the WM_CPM_CHM group were robustly higher than those of the WM group.Conclusion:Compared with WM alone,supplementing CPM and CHM to WM provides significant health benefits of improving the chance of recovered and improved outcome,and reducing the death rate,at an expense of longer LOS and higher CPS.     

Effects of Electroacupuncture on Hippocampal and Cortical Apoptosis in A Mouse Model of Cerebral Ischemia-reperfusion Injury

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.     

缺血性脑卒中的中医药治疗研究进展

缺血性脑卒中属于中医缺血性"中风"的范畴,具有发病率高、致残率高、预后差、易复发等特点。中医药治疗缺血性中风颇具优势,积累了丰富的理论知识和治疗经验。现就近年来中医药治疗缺血性脑卒中研究进展综述如下。     

缺血性中风中医药治疗近况

综述了近年来中医药对缺血性中风的治疗近况,主要从病因病机及辨证论治、专方专药、针灸治疗应用的临床研究几个方面进行总结,认为中医药治疗缺血性中风对减少患者致残率、提高生存质量和回归家庭社会有较好的作用,并对今后的发展提出了方向。     

Radix Kansui Stir-Fried with Vinegar Reduces Radix Kansui-Related Hepatotoxicity in Mice via Mitochondrial Pathway

Objective To investigate the mechanism of Radix Kansui(RK)stir-fried with vinegar(VRK)decreased hepatotoxicity in mice.Methods According to a random number table,40 mice were randomly divided into negative control group(0.5%carboxymethylcellulose sodium,20 mL/kg),positive control group(0.1%mixture of carbon tetrachloride in soybean oil,20 mL/kg),RK group(the ethyl acetate extracts of RK,250 g crude drug/kg)and VRK group(the ethyl acetate extracts of VRK,250 g crude drug/kg)with 10 mice per group.All mice were administered orally by gavage daily for 7 continuous days.The morphology of liver tissues was examined to assess the liver injury by a transmission electron microscope.Hepatocyte apoptosis in vivo was determined by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nickend labeling(TUNEL)assay.Immunohistochemical technique was adopted to detect the expression of particular antiapoptotic and proapoptotic proteins in the mitochondrial pathways,including B-cell lymphoma(Bcl-2)and caspase-3,as well as the expression of inflammatory mediators,including nuclear factor kappa B(NF-κB)and intercellular adhesion molecule-1(ICAM-1).Results Liver injury and hepatocyte apoptosis were observed in RK mice,and the liver injury were significantly reduced in VRK-treated mice.In immunohistochemistry study,compared with the negative control group,RK inhibited dramatically the Bcl-2 protein expression and significantly increased the expression of caspase-3,NF-κB and ICAM-1(all P<0.01).Compared with the RK group,VRK group induced significant increase on Bcl-2 protein expression,and decreased the caspase-3,NF-κB and ICAM-1 protein expression(P<0.05 or <0.01).Conclusion The mechanism of reduced hepatotoxicity of VRK may be associated with the reduced inflammation,regulation of antiapoptotic and proapoptotic mediators in the mitochondrial pathway.     

丙泊酚及缺血预处理对大鼠肝缺血－再灌注损伤时细胞凋亡的影响

目的：探讨丙泊酚及缺血预处理对大鼠肝脏缺血－再灌注损伤时细胞凋亡的影响。方法：成年健康SD大鼠72只，随机分为4组：假手术组（Sham组）、缺血－再灌注组（IR组）、缺血预处理组（IP组）、丙泊酚组（P组）。制作70％肝脏缺血－再灌注模型，实验结束后即刻取肝左叶。用免疫组化法检测Bcl-2与Bax蛋白表达量，TUNEL法检测肝细胞凋亡指数（AI）。结果：与Sham组比较，各组肝组织Bcl-2、Bax蛋白表达水平、凋亡指数均增加（P〈0．05）；与IR组比较，IP、P组Bcl-2蛋白表达增加、Bax蛋白表达和AI减少（P〈0．05）；与IP组比较，P组Bcl-2蛋白表达增加、Bax蛋白表达和AI减少（P〈0、05）。结论：丙泊酚及缺血预处理通过调节Bcl-2、Bax蛋白表达，使肝细胞凋亡减轻，对大鼠缺血再灌注肝脏可能有一定的保护作用。     

眼针联合电针、运动功能训练治疗缺血性卒中偏瘫患者的临床研究

目的 探究眼针联合电针、运动功能训练治疗缺血性卒中偏瘫患者的疗效及其磁共振弥散张量成像特征变化.方法 选择2018年3月至2020年3月我院收治缺血性卒中偏瘫患者180例,采用随机数字表法分为对照组(n=90)和观察组(n=90),对照组采用电针联合运动功能训练,观察组采用眼针、电针联合运动功能训练.观察2组患者的临床...     

大鼠局灶性脑缺血半暗带细胞凋亡动态变化规律的研究

用线栓法制作大鼠大脑中动脉阻塞 (MCAO)模型 ,然后用特异性细胞凋亡检测方法 (TUNEL法 ) ,对局灶缺血后不同时间点的脑组织进行观察。发现MCAO后各时间点局灶缺血范围内被标记的染色阳性的凋亡细胞主要位于局灶性缺血半暗带区 ,而且随着缺血时间的延长 ,凋亡细胞数逐渐增多 (缺血 1、3、6、1 2h分别为 3.6 0± 1 .0 2、1 5 .6 0± 2 .0 6、2 2 .4 0± 1 .85、33.0 0± 2 .83/mm2 ) ,2 4h达到高峰 ( 4 6 .6 0± 3.0 1 /mm2 ) ,4 8h以后明显减少 ( 1 3.6 0±2 .4 7/mm2 ) ,72h以后 ,凋亡表现逐渐消失 ( 5 .0 0± 1 .4 1 /mm2 ) ,各时间点的凋亡细胞数目有显著差异 (P <0 .0 1 ) ;同时两两比较表明除缺血后 1h与 72h,3h与 1 2h及 4 8h外 ,其余各点之间均有显著性差异 (P <0 .0 1 )。假手术组及对侧大脑半球各时间点基本上没有凋亡细胞出现。本研究从细胞凋亡角度重新认识急性缺血性脑血管病治疗的“时间窗” ,为缺血性卒中的治疗提供依据。     

中西医结合治疗缺血性中风126例辨治研究

目的：观察中西医结合治疗缺血性中风的临床疗效。方法：将126例缺血性中风患者随机分为两组，对照组采用溶栓、降纤、抗凝、抗血小板抑制剂、脑保护剂及对症治疗。治疗组在此基础上加以中医辨证分型予以中药治疗。两组进行神经功能缺损评分及临床疗效比较。结果：经治两个疗程，两组患者自身治疗前后对比均较治疗前有改善，对照组P〈0．05，治疗组P〈0．01；组间比较，治疗组的神经功能缺损评分改善情况优于对照组（P〈0．05）。治疗组总有效率97．22％，对照组88．89％。两组比较，差异有显著性意义，P〈0．01。结论：中西医结合治疗缺血性中风疗效优于单纯西医治疗。     

中医药治疗急性缺血性中风用药规律分析

目的:探讨中医药治疗急性缺血性中风用药规律分析。方法:运用知网、万方、维普数据库检索1996—2016年文献,最终符合标准的文献184篇,用EXCEL表格建立数据库,并分别对药物的使用次数、类别、功效、性味、归经、证型及治则治法运用SPSS统计学软件进行分析。结果:184篇文献中共使用中药132味,使用频次为1 760次。使用频次超过50次以上的中药依次为川芎、地龙、丹参、红花、赤芍、天南星、当归、桃仁、大黄、水蛭、半夏、石菖蒲、黄芪、天麻;其中活血化瘀药、熄风止痉药、补虚药居前3位;药性以温、寒、平为主,累计频率96.9%;药味以苦、甘、辛为主,累计频率88.0%;归经以入肝、心、脾、肺为主,累计频率97.8%:证型分布前3位者依次为痰瘀互阻型、气虚血瘀型、风痰瘀阻型。结论:急性缺血性中风治疗以痰瘀同治、补气活血化瘀、祛风化痰通络为主,其中常用活血化瘀、熄风止痉、补虚的药物,遵循痰瘀同治的原则。     

清脑方对缺血性眩晕大鼠脑损伤的保护作用

目的 初步研究清脑方（Qingnaofang, QNF）对缺血性眩晕大鼠脑损伤的保护作用及其作用机制。方法 采用手术结扎右侧颈总动脉和锁骨下动脉致大鼠右侧半脑不完全脑缺血建立缺血性眩晕大鼠模型。分为模型组,QNF 1.04、0.52、0.26 g/kg组,盐酸地芬尼多15 mg/kg组,银杏叶片5.76 mg/kg组以及假手术组,观察QNF对旋转刺激缺血性眩晕大鼠跳台逃避潜伏期的影响,取材并测定动物缺血侧组织Lac、LDH、SOD、MDA、NO及NOS的含量或活性。结果 （1）与模型组相比,QNF 1.04、0.52、0.26 g/kg组大鼠跳台逃避电击潜伏期分别缩短53.6%（P<0.01）、33.8%（P<0.05）、56.5%（P<0.01）。（2）QNF 1.04、0.52、0.26 g/kg均可显著降低缺血侧脑组织中Lac的含量以及LDH的活力 （P<0.05,P<0.01）,降低其TNOS及iNOS活力 （P<0.01）;QNF 0.52 g/kg剂量能够明显降低缺血侧脑组织中SOD活力;QNF 0.52、0.26 g/kg剂量可显著降低其MDA和NO的含量 （P<0.05,P<0.01）。结论 QNF对缺血性眩晕大鼠脑损伤有一定的保护作用,能够减轻模型动物的眩晕症状,其脑保护作用机制可能与改善缺血脑组织能量代谢,减少氧化应激和炎性损伤有关。     

高频电针配合中药倒模治疗囊肿型痤疮的疗效观察

目的:观察囊肿型痤疮治疗效果。方法:对照组(78例)常规用自制痤疮中药面膜倒模治疗,治疗组(120例)囊肿行高频电针打孔引流,囊腔内注入庆大霉素,再用痤疮中药面膜倒模治疗。结果:高频电针组痊愈79例,显效31例,总有效率为91.7%:对照组痊愈36例,显效22例,总有效率为74.4%:两组比较差异有统计学意义(χ2=11.01,P<0.01)。结论:高频电针配合中药倒模治疗重度囊肿型痤疮效果良好。     

中药抗脑缺血再灌注损伤机制及超微结构研究

目的:探索单剂中药组合对脑缺血/再灌注损伤机理。方法:Wistar雄性大鼠随机分为4组:中药组、尼膜通组、对照组及手术对照组。线栓法制作大鼠大脑中动脉可逆性脑缺血模型。再通前20min经尾静脉中药组注入丹参、川穹嗪和当归;尼膜通组注入尼膜通;对照组给予生理盐水。再通后12、24和36h重复给药。再通48h,提取分离白细胞,测定线粒体超氧化物歧化酶(SOD)活性;采用Western印迹法,测定鼠抗羊单克隆抗体(Calbidin)和鼠抗羊单克隆抗体(LFA-1)表达水平;电镜下观察超微结构。结果:中药组大鼠缺血区脑组织线粒体中SOD活性及Calbindin表达水平最高。而中药组LFA-1表达水平却最低。电镜结果表明,中药组缺血神经元、神经胶质细胞、血管内皮细胞损害及炎性细胞的血管黏附均最弱。结论:单剂中药组合通过抗炎、清除自由基、钙离子拮抗机制对脑缺血/再灌注损伤起到保护作用。     

急性缺血性脑卒中时胃黏膜细胞凋亡和胃屏障损伤的关系

目的评估缺血性脑卒中应激时胃黏膜细胞凋亡的状况,探讨胃黏膜细胞凋亡和胃屏障形态学和功能的关系。方法10只犬制作缺血性脑卒中模型,另10只伪手术对照。制模后检测胃蔗糖通透性,24h后取全胃行大体病理分级和组织学积分,同时测定胃黏膜上皮细胞凋亡指数。结果实验组和伪手术组相比,胃黏膜细胞凋亡显著增加(14·83±4·41vs·5·60±2·61,P<0·05);胃黏膜细胞凋亡和蔗糖通透性(r=0·89,P<0·05)、胃大体病理(r=0·87,P<0·05)、胃组织学积分(r=0·92,P<0·05)均呈正相关。结论缺血性脑卒中虽未造成全身循环呼吸等明显改变,但已引起细胞凋亡增加、胃黏膜屏障损伤,且细胞凋亡增加与屏障功能损伤、大体病理改变同步发生,提示屏障损伤的细胞基础可能与胃黏膜上皮细胞的加速凋亡相关。     

电针上调δ阿片受体的表达减轻大鼠急性缺血性脑损伤

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。