复方中药塞络通对多发性脑梗死大鼠星形胶质细胞功能及脂笼蛋白2蛋白表达的影响

目的脑卒中是一种常见的疾病,绝大多数脑卒中病例是由短暂性或永久性脑血管闭塞引起的缺血性脑血管病(缺血性中风)最终导致脑梗死。星形胶质细胞做为脑内大量存在的细胞,在缺血损伤后形态肥大,表现为突起延长和胞体肿胀。脂笼蛋白2(LCN2)是一种分泌蛋白,在脑缺血和神经退行性疾病中具有重要作用。塞络通胶囊(SLT)是由人参、银杏、藏红花三种中草药组成的治疗血管性痴呆的标准化制剂。虽然最近的临床试验已经证明SLT对血管性痴呆的有益作用,但其潜在的细胞机制尚未得到充分的探索。方法采用大鼠微球法致多发性脑梗死实验模型,通过Morris水迷宫实验评价SLT对恢复期大鼠空间记忆功能障碍的影响;随后,根据组织内及血清内炎性因子的表达,以及qPCR、免疫荧光、免疫印迹观察星形胶质细胞的活化、特异蛋白LCN2及其诱导的JAK2\STAT3信号通路的变化,以考察恢复期脑缺血损伤后星形胶质细胞的活化与炎性反应的关系及SLT对恢复期缺血损伤皮层区星形胶质细胞功能的影响;建立人星形胶质细胞糖氧诱导(OGD)损伤模型,并采用慢病毒转染的方法过表达目的基因LCN2,检测细胞分泌炎性因子含量变化,免疫荧光、蛋白免疫印迹观察星形胶质细胞的活化、特异蛋白LCN2及其诱导的JAK2/STAT3信号通路的变化,考察星形胶质细胞损伤后SLT有效成分对其的影响。结果 SLT可显著降低脑缺血引起的大鼠空间记忆认知功能障碍,减轻星形胶质细胞的活化及增殖,较为明显改善脑脑缺血损伤大鼠皮层缺血周边半暗带区神经元及突触超微结构损伤;SLT可抑制缺血侧皮层区及血清内炎性因子及趋化因子的表达,根据免疫荧光与免疫印迹的结果看出,SLT可能通过抑制LCN2诱导的JAK2/STAT3信号通路的表达来抑制炎性反应。结论 SLT介导神经炎症反应,通过LCN2-JAK2/STAT3通路抑制星形胶质细胞增生,抑制神经炎症反应,从而保护缺血性脑损伤,为缺血性脑卒中的治疗策略提供新的思路。     

心脉通胶囊对脑梗死恢复期患者血脂、血流变的影响

目的：观察心脉通胶囊对恢复期脑梗死的治疗效果。方法治疗组60例脑梗死恢复期病人,在常规拜阿司匹林片加阿托伐他钙片治疗的基础上口服心脉通胶囊治疗,1次3粒,1日3次,3月为1个疗程。同时设对照组60例脑梗死恢复期病人,采用常规治疗。观察两组患者的症状,体症及血流变学、血脂变化指标。结果治疗组60例,显效29例,有效26例,无效6例,总有效率91．7％,与对照组比较,两组有效率差异有统计学意义（ P＜0．05）。结论心脉通胶囊对脑梗死恢复期具有很好的临床使用价值,并能有效的降低患者的全血黏度及血脂,保护血管内皮功能。     

蛭蛇通络胶囊联合血栓通注射液治疗脑梗死恢复期临床评价

目的探讨蛭蛇通络胶囊联合血栓通注射液治疗脑梗死恢复期的临床疗效。方法选取医院2016年2月至2017年12月收治的脑梗死恢复期患者200例,按随机数字表法分为对照组(99例)和研究组(101例)。两组患者均给予血栓通注射液治疗,研究组患者加用蛭蛇通络胶囊治疗。两组均治疗4周。结果研究组总有效率为89. 11%,显著高于对照组的73. 74%(P <0. 05);治疗后,两组患者的中医症候积分均低于治疗前,且研究组低于对照组(P <0. 05);两组患者的高切还原黏度(HSRV)、全血黏度(WBV)、低切还原黏度(LSRV)、血液沉降率(ESR)、纤维蛋白原(FIB)及总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)均较治疗前降低(P <0. 05),且研究组患者的WBV,ESR,FIB及TC,TG,LDL-C均低于对照组患者(P <0. 05),但两组患者的高密度脂蛋白胆固醇(HDL-C)高于治疗前,且研究组高于对照组(P <0. 05);两组不良反应发生率相当(P> 0. 05)。结论蛭蛇通络胶囊联合血栓通注射液治疗脑梗死恢复期的临床疗效较好,可改善患者的中医症候积分、血液流变学及血脂水平,且安全性较高。     

灯银脑通胶囊联合脑心通胶囊治疗脑梗死恢复期的疗效观察

目的探究灯银脑通胶囊联合脑心通胶囊治疗脑梗死恢复期的临床疗效。方法选取2013年1月—2016年1月在天津中医药大学第一附属医院接受治疗的脑梗死恢复期患者85例,随机分为对照组(43例)和治疗组(42例)。对照组口服脑心通胶囊,3粒/次,3次/d。治疗组在对照组基础上口服灯银脑通胶囊,3粒/次,3次/d。两组患者均治疗3个月。观察两组的临床疗效,比较两组的美国国立卫生研究院卒中量表(NIHSS)评分、Barthel指数评分和生活质量的情况。结果治疗后,对照组和治疗组的总有效率分别为60.47%、80.95%,两组比较差异有统计学意义(P0.05)。治疗后,两组NIHSS评分均明显降低,而Barthel指数评分均显著升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组生理功能(PF)、生理职能(RP)、情感职能(RE)、社会功能(SF)、躯体疼痛(BP)、机体活力(VT)、精神健康(MH)和总体健康(GH)评分均显著升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的升高程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。结论灯银脑通胶囊联合脑心通胶囊治疗脑梗死恢复期具有较好的临床疗效,能明显改善神经功能和生活能力,提高生活质量,具有一定的临床推广应用价值。     

豨莶通栓胶囊联合长春西汀治疗脑梗死恢复期的疗效观察

目的 观察豨莶通栓胶囊联合长春西汀片治疗脑梗死恢复期的临床疗效。方法 选取2019年3月—2021年2月开封市中心医院收治的150例脑梗死恢复期患者,采用随机数字表法将患者分为对照组和治疗组,每组各75例。对照组饭后0.5 h口服长春西汀片,1片/次,3次/d。治疗组在对照组基础上饭后0.5 h口服豨莶通栓胶囊,3粒/次,3次/d。两组患者均连续治疗3个月。观察两组疗效,比较两组患者神经功能缺损情况、日常生活活动能力、脑血流动力学参数、血液流变学。结果 治疗后,治疗组的总有效率为90.67%,高于对照组的总有效率74.67%,差异有统计学意义（P<0.05）。治疗后,两组美国国立卫生研究院脑卒中量（NIHSS）评分较治疗前降低,Barthel指数较治疗前升高（P<0.05）,且治疗组的NIHSS评分、Barthel指数改善效果更明显（P<0.05）。治疗后,两组阻力指数（RI）、搏动指数（PI）较治疗前降低,平均血流速度（V_m）较治疗前升高（P<0.05）,且治疗组的脑血流动力学参数改善效果更明显（P<0.05）。治疗后,两组纤维蛋白原、血浆比黏度、D-二聚体较治疗前降低（P<0.05）,治疗组的纤维蛋白原、血浆比黏度、D-二聚体均明显低于对照组（P<0.05）。结论 豨莶通栓胶囊联合长春西汀片治疗脑梗死恢复期的疗效较好,可提高患者日常生活能力,减轻脑神经功能缺损,进一步改善脑血流动力学参数和血液流变学,具有一定的临床应用价值。     

通心络联合天丹通络胶囊治疗恢复期脑梗死42例

目的观察通心络联合天丹通络胶囊治疗恢复期脑梗死的疗效。方法将84例恢复期脑梗死患者,随机分为治疗组和对照组。治疗组42例口服通心络胶囊每次3粒、3次／天,天丹通络胶囊每次5粒、3次／天;对照组42例口服脑脉泰胶囊,每次2粒,3次／天。均以30（1为1个疗程,于2个疗程后判断疗效。结果治疗组基本治愈率14．29％,显效率61．90％,有效率23．81％。对照组基本治愈率7．14％,显效率33．33％,有效率59．53％。两组总有效率均为100．00％。两组基本治愈、显效率比较差并有统计学意义（P〈0．01）,总有效率比较差异无统计学意义（P〉0．05）。结论通心络联合天丹通络胶囊是治疗恢复期脑梗死的有效药物。     

通络救脑注射液对脑缺血大鼠脑皮质梗塞灶Glu及其NMDA受体表达的影响

目的：观察通络救脑注射液对脑缺血大鼠脑皮质梗塞灶Glu及其NMDA受体表达的影响。方法：采用三氯化铁致大脑中动脉血栓形成大鼠脑缺血模型，免疫组织化学方法及图像分析，统计使用t检验。结果：模型组大鼠脑皮质梗塞灶Glu及其NMDA受体表达与假手术对照组比较明显增强，通络救脑注射液各组大鼠脑皮质梗塞灶Glu及其NMDA受体表达与模型组比较明显降低。结论：通络救脑注射液能明显降低Glu及NMDA受体在脑缺血大鼠脑皮层梗塞灶的表达。     

中药复方胶囊对多发性脑梗死痴呆大鼠的影响

目的：观察中药复方胶囊（YSYN）对大鼠多发性脑梗死痴呆（MID）的疗效及作用机制。方法于左侧颈外动脉注入复合血栓诱导剂,复制多发性脑梗死痴呆模型。采用Morris水迷宫法进行学习记忆测试;采用酶联免疫法测定海马组织去甲肾上腺素（NE）水平;采用比色法测定海马组织乙酰胆碱酯酶（AchE）、乙酰胆碱转移酶（CHAT）和谷胱甘肽过氧化物酶（GSH-Px）水平。结果 YSYN能够显著提高多发性脑梗死痴呆大鼠学习记忆能力（P＜0．05）;显著降低多发性脑梗死痴呆大鼠海马组织AchE含量,提高多发性脑梗死痴呆大鼠海马组织CHAT、NE及GSH-Px含量（P＜0．05～0．01）。结论 YSYN能够显著改善多发性脑梗死痴呆大鼠的学习记忆功能,对MID具有较好的保护作用,其作用机制可能是通过调节海马组织内NE、Ach（乙酰胆碱）及GS H （谷胱甘肽）的活性来实现的。     

通心络胶囊治疗脑梗死恢复期的临床观察

目的：探讨通心络胶囊应用于脑梗死恢复期的临床疗效。方法选取98例脑梗死恢复期的患者并按照治疗顺序随机均分为对照组及治疗组各49例,在临床治疗方面,对照组患者采用银杏叶片,治疗组采用通心络胶囊,将两组患者治疗4周后的血脂变化、血液流变学的指标以及临床疗效进行对照比较。结果治疗组在血脂变化、血液流变学指标以及临床疗效等方面与对照组相比较,差异均具有统计学意义（P〈0.05）。结论通心络胶囊应用于脑梗死恢复期患者的临床治疗当中,能够显著调节血脂,改善血液流变学指标,疗效显著,值得临床应用及推广。     

康脑液预处理对脑缺血再灌注损伤大鼠脑组织的谷氨酸/氨基丁酸比值的影响

目的 观察康脑液对局灶性脑缺血再灌注损伤大鼠脑组织中氨基酸类神经递质的的影响.方法 将60只大鼠随机分为6组:假手术组,模型组,康脑液低、中、高剂量组,依达拉奉组.用栓线法复制大鼠大脑中动脉栓塞模型,缺血2h再灌注1h后,断头取脑,用2,4-二硝基氟苯柱前衍生法,测定大鼠脑组织中Glu与γ-GABA含量.结果 与假手术组相比,模型组大鼠脑组织中Glu和γ -GABA含量均明显上升,Glu/GABA明显升高(P＜0.05);与模型组比较,康脑液能够不同程度地降低大鼠脑组织中Glu含量,降低γ-GABA含量,使Glu/GABA趋于正常,具有显著性差异(P＜0.05).结论 康脑液可能通过降低缺血再灌注损伤大鼠脑组织中Glu含量及Glu/GABA比值从而发挥脑保护作用.     

Effect of antidepressants on GABA(B) receptor function and subunit expression in rat hippocampus

Laboratory and clinical studies suggest that depression is associated with changes in the hippocampus and that this brain region is a major target for antidepressant drugs. Given the data suggesting that GABA(B) receptor antagonists display antidepressant properties, the present study was undertaken to assess the effect of antidepressant administration on GABA(B) receptors in the rat hippocampus to determine whether changes in this regional receptor system may play a role in the response to these agents. Rats were administered (i.p.) the monoamine oxidase inhibitors tranylcypromine (10mg/kg) or phenelzine (10mg/kg), the tricyclic antidepressant desipramine (15 mg/kg), or fluoxetine (5mg/kg), a selective serotonin re-uptake inhibitor, once daily for seven consecutive days. Two hours following the last drug treatment the hippocampal tissue was prepared for defining the distribution and quantity of GABA(B) receptor subunits using in situ hybridization and for assessing GABA(B) receptor function by quantifying baclofen-stimulated [(35)S]-GTPgammaS binding. All of these antidepressants selectively increased the expression of the GABA(B(1a)) subunit in hippocampus, having no consistent effect on the expression of GABA(B(1b)) or GABA(B(2)). Moreover, except for fluoxetine, these treatments increased GABA(B) receptor function in this brain region. The results indicate that an enhancement in the production of hippocampal GABA(B(1a)) subunits may be a component of the response to antidepressants, supporting a possible role for this receptor in the symptoms of depression and the treatment of this condition.     

On the involvement of multiple muscarinic receptor subtypes in the activation of phosphoinositide metabolism in rat cerebral cortex

We have examined the activation of phosphoinositide metabolism by muscarinic agonists in rat cerebral cortex, in an attempt to delineate the mechanisms by means of which some selective antagonists inhibit this response in a manner that deviates from simple mass action law. The accumulation of [3H]inositol phosphates induced by the full agonist carbamylcholine in cell aggregates preparations was inhibited by muscarinic antagonists with the following order of potency: telenzepine greater than atropine greater than 4-diphenylacetoxy-N-methyl-piperidine methbromide greater than pirenzepine greater than hexahydro-sila-difenidol greater than AF-DX 116. The same order of potency was found for the competition of these antagonists with [3H]telenzepine binding to M1 muscarinic receptors. The inhibition of the formation of [3H]inositol phosphates activated by acetylcholine, carbamylcholine, and oxotremorine-M by pirenzepine and telenzepine showed biphasic curves, with 62-73% of the response being inhibited with high affinity. Atropine, AF-DX 116, and pirenzepine shifted the concentration-response curves of oxotremorine-M to the right in a parallel manner. However, pirenzepine at micromolar concentrations showed deviation from linearity of the Schild regression. The blockade by high concentrations of pirenzepine and telenzepine showed less than additive dose ratios when assayed in the presence of atropine, suggesting deviation of their antagonism from simple competition. However, after alkylation with propylbenzilylcholine mustard in the presence of low concentrations of pirenzepine, the response to carbamylcholine and oxotremorine-M showed monophasic inhibition curves by pirenzepine and linear Schild regression for this antagonist. These results support the interpretation that the formation of [3H]inositol phosphates is activated by multiple muscarinic receptor subtypes in rat cerebral cortex. The profile of affinities of muscarinic antagonists indicates that a major component of the response is activated by an M1 receptor subtype and a minor component is probably mediated by M3 muscarinic receptors when acetylcholine, carbamylcholine, or oxotremorine-M are used to stimulate the response. Conversely, pirenzepine inhibited the response induced by methacholine and bethanechol in a monophasic manner with high affinity (Ki = 13 nM), suggesting that these agonists can selectively stimulate phosphoinositide metabolism through activation of M1 muscarinic receptors in rat cerebral cortex.     

Effects of GABA and various allosteric ligands on TBPS binding to cloned rat GABA(A) receptor subtypes.

1. [35S]t-butylbicyclophosphorothionate (TBPS) is a high affinity ligand for the picrotoxin site of GABA(A) receptors. Here we examined TBPS binding to the cloned receptors made of alpha 1, alpha 3 or alpha 6 in combination with beta 2 or beta 2 and gamma 2 subunits, in the presence of GABA and several allosteric ligands (diazepam, methyl 6,7-dimethoxy-4-methyl-beta-carboline-3-carboxylate (DMCM), 3 alpha,21-dihydroxy-5 alpha-pregnan-20-one (5 alpha-THDOC), pentobarbitone and Zn). The cloned receptors were transiently expressed in SF-9 insect cells by infecting with recombinant baculoviruses. 2. In alpha beta subtypes, GABA at nanomolar concentrations enhanced TBPS binding but inhibited binding at micromolar concentrations. Half maximal GABA concentrations for enhancement or inhibition of TBPS binding were correlated with high and low affinity GABA binding sites, respectively, in individual subtypes. The maximal enhancement of binding also varied according to the alpha isoform (alpha 3 beta 2 >> alpha 1 beta 2). In alpha beta gamma subtypes, TBPS binding was unaffected by GABA at nanomolar concentrations, but was inhibited by GABA at micromolar concentrations. Addition of gamma 2 thus appeared to abolish conformational coupling between high affinity GABA sites and TBPS sites, and also altered low affinity GABA sites; in particular, the half maximal GABA concentration for inhibition of TBPS binding changed from > 100 (alpha 6 beta 2) to 1 microM (alpha 6 beta 2 gamma 2). 3. Allosteric ligands also altered TBPS binding to sensitive GABA(A) receptor subtypes.(ABSTRACT TRUNCATED AT 250 WORDS)     

NMDA receptor characterization and subunit expression in rat cultured mesencephalic neurones

1. NMDA-induced changes in free intracellular Ca2+ concentration ([Ca2+]i) were determined in individual cultured rat mesencephalic neurones by the fura-2 method. mRNA expression encoding NMDA receptor subunits (NR1, NR2A-D) was examined by RT-PCR. 2. NMDA (1-100 microM, plus 10 microM glycine) induced a concentration-dependent increase in [Ca2+]i (EC50 = 5.7 microM). The effect of NMDA was virtually insensitive to tetrodotoxin (0.3 microM) and nitrendipine (1 microM), but dependent on extracellular Ca2+. 5,7-Dichlorokynurenic acid (10 microM), a specific antagonist at the glycine binding site on the NMDA receptor, abolished the NMDA response. 3. Memantine, an open-channel blocker, and ifenprodil, a preferential non-competitive NR1/NR2B receptor antagonist diminished the NMDA effect with an IC50 value of 0.17 and 1 microM, respectively. Ethanol at 50 and 100 mM caused about 25 and 45%-inhibition, respectively. 4. Agarose gel analysis of the PCR products followed by ethidium bromide fluorescence or CSPD chemiluminescence detection revealed an almost exclusive expression of the NR1 splice variants lacking exon (E) 5 and E22. The 3' splice form without both E21 and E22 exceeded that containing E21 by approximately 4 fold. The relative amounts of NR2A, NR2B, NR2C corresponded to approximately 1:2:1. NR2D mRNA was also detectable. 5. In conclusion, mesencephalic neurones bear ethanol-sensitive NMDA receptors which might be involved in the development of ethanol dependence and withdrawal. The high affinity of NMDA to this receptor, its sensitivity to ifenprodil and memantine may suggest that the mesencephalic NMDA receptor comprises the NR1 splice variant lacking E5, NR2B, and NR2C, respectively.     

清心饮加减对脑梗死患者血浆PAF、GMP-140的影响及临床效果研究

目的观察清心饮加减治疗脑梗死的临床疗效以及对其血浆GMP-140、PAF水平的影响。方法选取我院2014年2月~2015年5月收治的脑梗死患者108例,采用随机法分为观察组和对照组。对照组给予阿司匹林联合阿托伐他汀等常规治疗,观察组给予阿司匹林、阿托伐他汀加清心饮加减治疗。两组均治疗15d。观察两组治疗前后血浆GMP-140、PAF水平变化。观察3个月后两组的临床疗效及中医症候疗效。结果治疗15d后观察组与对照组GMP-140水平分别为(19.94±5.89)μg/L和(24.56±9.34)μg/L,血浆PAF水平分别为(88.45±10.32)ng/m L和(100.23±12.34)ng/m L.两组治疗后GMP-140、PAF水平均较治疗前降低(P<0.05)。治疗后,观察组GMP-140、PAF水平均低于对照组(P<0.05)。3个月后,观察组的临床疗效及中医症候疗效均优于对照组(P<0.05)。结论清心饮加减能够降低血浆PAF、GMP-140水平,有效促使脑神经功能恢复。     

Modulation of NMDA receptor by huperzine A in rat cerebral cortex 1

目的：研究石杉碱甲（ＨｕｐＡ）对大脑皮层ＮＭＤＡ受体的影响．方法：１）用急性分离海马锥细胞全细胞记录研究ＨｕｐＡ对ＮＭＤＡ诱发电流的影响．２）用大脑皮层突触膜标本研究ＨｕｐＡ对［３Ｈ］Ｄｉｚ特异性结合的影响．结果：１）ＨｕｐＡ可逆地抑制ＮＭＤＡ诱发的电流反应（ＩＣ５０＝４５４μｍｏｌ·Ｌ－１）．２）在突触膜标本,ＨｕｐＡ抑制［３Ｈ］Ｄｉｚ的结合量（ＩＣ５０＝０５（０１－１９）μｍｏｌ·Ｌ－１,ｎ＝４）．３）Ｌ谷氨酸１０μｍｏｌ·Ｌ－１增加［３Ｈ］Ｄｉｚ结合量．加入Ｌ谷氨酸后,ＨｕｐＡ０００１－０１μｍｏｌ·Ｌ－１进一步增加结合量;ＨｕｐＡ１－３００μｍｏｌ·Ｌ－１则抑制结合量（ＩＣ５０＝１２３（５８－２６３）μｍｏｌ·Ｌ－１,ｎ＝５）．结论：ＨｕｐＡ在大脑皮层除了抑制乙酰胆碱酯酶外,还是ＮＭＤＡ受体拮抗剂     

石杉碱甲对大鼠大脑皮层NMDA受体的调制作用

AIM: To investigate the effects of huperzine A (Hup A) on NMDA receptors in rat cerebral cortex. METHODS: 1) The effect of hup A on NMDA-induced current was studied in acutely dissociated rat hippocampal pyramidal neurons using whole-cell recording. 2) The effect of Hup A on NMDA receptor binding was assessed using [3H] dizocilpine (Diz) binding assay in synaptic membrane preparation of rat cerebral cortex. RESULTS: 1) Hup A reversibly inhibited NMDA-induced current in a concentration-dependent manner with IC50 of 45.4 mumol.L-1. 2) Hup A inhibited the specific binding of [3H]MK-801 to extensively washed synaptic membrane of rat cerebral cortex in a concentration-dependent manner with IC50 of 0.5 (0.1-1.9) mumol.L-1 (n = 4). 3) L-Glutamate 10 mumol.L-1 markedly increased [3H] MK-801 binding. In the presence of L-glutamate, Hup A 0.001-0.1 mumol.L-1 caused a further increase of the binding, whereas Hup A 1-300 mumol.L-1 inhibited the binding in a concentration-dependent manner with IC50 of 12.3 (5.8-26.3) mumol.L-1 (n = 5). CONCLUSION: Hup A acted as an antagonist of NMDA receptor in cerebral cortex in addition to its inhibitory effect on acetylcholinesterase.     

丁苯酞软胶囊对脑梗死血流灌注情况及记忆运动的改善作用

目的探究丁苯酞软胶囊对脑梗死血流灌注情况及记忆运动的改善作用。方法随机选取187例轻度认知功能障碍的脑梗死患者,根据随机数表法均分为对照组与观察组,对照组给予常规治疗,观察组在对照组的基础上联合丁苯酞软胶囊治疗。观察并比较两组临床疗效、血清中细胞因子(TNF-α、IL-18)及NSE的变化情况,CT脑灌注成像结果,缺血低灌注面积,蒙特利尔认知评估量表评分。结果治疗后,观察组临床疗效总有效率为93.61%,显著高于对照组的81.72%(P<0.05);观察组TNF-α[(8.21±1.13)mg/L]、IL-18[(78.16±24.47)pg/ml]、NSE[(23.85±5.02)ng/L]水平均显著低于对照组[TNF-α(10.87±2.16)mg/l、IL-18(96.27±26.17)pg/ml、NSE(31.72±5.17)ng/L](P<0.05);观察组缺血低灌注区面积[(1 629.68±1 078.17)mm~2]显著低于对照组[(2 825.46±1 115.63)mm~2](P<0.05);观察组CBF[(76.43±13.57)ml/100 mg]、CBV[(95.17±9.03)ml/100 mg]显著高于对照组[CBF(55.27±14.19)ml/100 mg、CBV(84.63±8.48)ml/100 mg](P<0.05);治疗后MoCA评分观察组(27.09±2.49)分、对照组(24.11±3.08)分,均较本组治疗前显著升高,进一步组间比较,观察组治疗后MoCA评分显著高于对照组。观察组MoCA评分疗效显效、有效例数均多于对照组(P<0.05)。结论丁苯酞软胶囊应用于脑梗死患者治疗中,能显著改善血流灌注情况,恢复记忆运动功能。     

遗传性癫痫易感大鼠脑内NMDA受体功能的研究

Ｎ－甲基－Ｄ－天门冬氨酸（ＮＭＤＡ）受体与癫痫的产生密切相关，我们以［３Ｈ］ＭＫ－８０１在ＮＭＤＡ受体激动剂作用下与突触膜结合情况，检测了遗传性癫痫易感大鼠Ｐ７７ＰＭＣ的ＮＭＤＡ受体功能。结果显示：１０－６ｍｏｌ·Ｌ－１谷氨酸或１０－６ｍｏｌ·Ｌ－１谷氨酸加１０－６ｍｏｌ·Ｌ－１甘氨酸可促进Ｐ７７ＰＭＣ大鼠大脑皮层、海马对［３Ｈ］ＭＫ－８０１的结合，并显著高于对照。一些抗癌药及生物制剂可降低或促进［３Ｈ］ＭＫ－８０１的结合。提示ＮＭＤＡ受体活性增高是遗传性癫痫易感大鼠惊厥产生的重要因素，以及抗病药的可能作用途径。