Neuroprotective effect ofShenqi Fuzheng injection pretreatment in aged rats with cerebral ischemia/reperfusion injury

Shenqi Fuzheng injection is extracted from the Chinese herbs Radix Astragali and Radix Codonopsis. The aim of the present study was to investigate the neuroprotective effects of Shenqi Fuzheng injection in cerebral ischemia and reperfusion. Aged rats(20–22 months) were divided into three groups: sham, model, and treatment. Shenqi Fuzheng injection or saline(40 m L/kg) was injected into the tail vein daily for 1 week, after which a cerebral ischemia/reperfusion injury model was established. Compared with model rats that received saline, rats in the treatment group had smaller infarct volumes, lower brain water and malondialdehyde content, lower brain Ca2+ levels, lower activities of serum lactate dehydrogenase and creatine kinase, and higher superoxide dismutase activity. In addition, the treatment group showed less damage to the brain tissue ultrastructure and better neurological function. Our findings indicate that Shenqi Fuzheng injection exerts neuroprotective effects in aged rats with cerebral ischemia/reperfusion injury, and that the underlying mechanism relies on oxygen free radical scavenging and inhibition of brain Ca2+ accumulation.     

适度酒精预适应对大鼠局灶性脑缺血再灌注损伤保护作用的研究

目的 研究适度酒精预适应对大鼠局灶性脑缺血再灌注诱导的神经元损伤的保护作用。 方法 将36只雄性SD大鼠随机分为假手术组、缺血再灌注组和酒精预适应组,每组12只。局灶性脑 缺血再灌注模型采用右侧大脑中动脉闭塞方式,缺血2 h,再灌注24 h。酒精预适应组在脑缺血再灌 注前24 h用95%酒精与0.3 ml无菌蒸馏水混合后进行灌胃,95%酒精体积（μl）计算为：[大鼠体重（g） x0.6]+0.3。其余两组用同等剂量的生理盐水灌胃。每组取8只大鼠在缺血再灌注后24 h进行神经功能 评分和氯化2,3,5-三苯基四氮唑（2,3,5-Triphenyltetrazolium chloride,TTC）染色并根据染色结果计 算脑梗死体积。每组剩余的4只,在缺血再灌注后24 h进行磁共振T2加权像（T2-weighted imaging,T2WI） 序列扫描,然后将大鼠处死取脑,经过冷冻切片后,每只大鼠取第一躯体感觉皮质区的2张切片,1 张用末端转移酶介导的脱氧尿嘧啶核苷三磷酸缺口末端标记（terminal deoxynucleotidyl transferasemediated 2'-deoxyuridine 5'-triphosphate nick-end labeling,TUNEL）检测其凋亡性细胞死亡情况,另一 张用Fluoro-Jade B检测其神经元退化变性情况。 结果 相较于缺血再灌注组,经过适度酒精预适应后会显著降低大鼠的神经功能评分[15.00 （14.25,16.00）vs 3.50（2.25,4.00）（P <0.001）]、脑梗死体积[TTC：（242.80±17.44）mm3 vs （54.83±13.43）mm3;T2WI ：（296.80±8.53）mm3 vs（59.68±9.97）mm3,P均<0.001]、凋亡细胞所占百 分比[（33.47±2.23）% vs（9.66±0.84）%,P <0.001]和退化变性神经元所占百分比（[ 45.31±3.40）% vs（23.26±1.25）%,P <0.001]。 结论 适度酒精预适应可以保护局灶性脑缺血再灌注诱导的神经元损伤。     

缺血后处理对大鼠局灶性脑缺血再灌注损伤热休克蛋白70影响

目的探讨缺血后处理(Postcond)对大鼠局灶性脑缺血再灌注损伤热休克蛋白70(HSP70)表达的影响,以探讨其脑保护的机制。方法成年健康SD大鼠45只,随机分为假手术组、缺血再灌注组、缺血后处理组,应用线栓法建立大脑中动脉闭塞(MCAO)再灌注模型,于灌注24h后断头留取大脑皮质组织,用免疫组化、Western blot检测HSP70蛋白的含量;逆转录聚合酶链反应(RT-PCR)方法检测HSP70mRNA表达水平。结果局灶性脑缺血再灌注24h后脑皮质内HSP70mRNA和HSP70蛋白的表达增加(P0.05)。应用缺血后处理能显著地促进脑缺血再灌注后脑组织HSP70mRNA和HSP70蛋白的表达(P0.05)。结论缺血后处理促进大鼠局灶性脑缺血再灌注皮质内HSP70的表达,这可能是其脑保护作用的部分机制。     

阿斯匹林干预对沙鼠脑缺血再灌注后NF-κB、MCP-1表达的影响

目的 通过研究阿斯匹林干预对沙鼠脑缺血再灌注后NF-κB、MCP-1表达的影响，旨在进一步探讨阿斯匹林在脑缺血再灌注损伤中的作用。方法 将50只健康蒙古沙鼠随机分为正常对照组、假手术组、脑缺血再灌注组（I／R组）、阿斯匹林干预组；夹闭双侧颈总动脉10min后松夹，建立沙鼠全脑缺血再灌注模型；用免疫组化法检测缺血脑组织NF-κBp65、MCP-1的表达。结果缺血再灌注后6h～7d NF-κBp65的表达量显著高于正常对照组及假手术组（P〈0．01），且出现MCP-1阳性表达；同I／R组比较，阿斯匹林干预组在缺血再灌注后6h、1d、3d、7d NF-κBp65与MCP-1表达量均下降（P〈0．05）。结论 阿斯匹林能够下调NF-κB、MCP-1的表达而减轻脑缺血再灌注损伤。     

大鼠局灶性缺血再灌注后大脑皮质ADM及其mRNA的表达

目的探讨肾上腺髓质素（ADM）与脑缺血再灌注损伤的关系。方法采用线栓法制成大鼠大脑中动脉缺血再灌注模型，阻断血流2h进行再灌注。应用免疫组织化学法和RT—PCR法检测不同时间段大鼠局灶性脑缺血再灌注后大脑皮质ADM及其mRNA的表达，并进行动态观察。结果正常大鼠大脑皮质有ADM及其mR—NA的表达，假手术组ADM及其mRNA表达略高于正常组，P〉0．05；大鼠脑缺血再灌注后大脑皮质ADM及其mRNA过表达，与正常对照组及假手术组相比差异显著，P〈0．05。动态观察发现，脑缺血2h再灌注2h，大脑皮质ADM及其mRNA即表达，再灌注22h达高峰，至1w仍明显多于正常对照组，P〈0．05。结论脑缺血再灌注后ADM及其mRNA呈现规律性过表达。     

Effects of transection of cervical sympathetic trunk on cerebral infarct volume and oxygen free radical levels in rats with focal cerebral ischemia/reperfusion injury

BACKGROUND: Stellate ganglion block (SGB) plays a protective role on the brain, but the precise mechanism of action is not clear.OBJECTIVE: To simulate SGB by transection of the cervical sympathetic trunk (TCST) and to investigate the TCST effects on changes in cerebral infarct volume and oxygen free radical levels in rats with focal cerebral ischemia/reperfusion injury.DESIGN, TIME AND SETTING: A complete randomized control animal experiment was performed at the Institute of Neurological Diseases of Taihe Hospital, Yunyang Medical College from February to December 2005.MATERIALS: A total of 101 healthy Wistar rats, weighing 280-320g, of both genders, aged 17-18 weeks, were used in this study. 2,3,5-triphenyltetrazolium chloride (TTC) was purchased from Changsha Hongyuan Biological Company. Superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) assay kits were provided by Nanjing Jiancheng Bioengineering Institute.METHODS: Rats were randomly divided into a TCST group, a model group and a sham operation group. Successful models were included in the final analysis, with at least 20 rats in each group. After TCST, rat models of focal cerebral ischemia/reperfusion injury were established in the TCST group by receiving middle cerebral artery occlusion (MCAO) by the intraluminal suture method for 2 hours, followed by 24 hours of reperfusion. Rat models of focal cerebral ischemia/reperfusion injury were made in the model group. Rats in the sham operation group underwent experimental procedures as for the model group, threading depth of 10mm, and middle cerebral artery was not ligated.MAIN OUTCOME MEASURES: Brain tissue sections of ten rats from each group were used to measure cerebral infarct volume by TTC staining. Brain tissue homogenate of another ten rats from each group was used to detect SOD activities, MDA contents and NO levels. Rat neurological function was assessed by neurobehavioral measures.RESULTS: Cerebral infarct volume was bigger in the model group than in the TCST group (P<0.05). Twenty four hours after cerebral ischemia/reperfusion, SOD activities were lower, whereas MDA contents and NO levels were higher in the TCST and model groups, compared with the sham operation group (P<0.05 or P<0.01). Compared with the model group, SOD activities were higher, whereas MDA contents and NO levels were lower in the TCST group (P<0.05).CONCLUSION: After TCST, cerebral infarct volume is reduced, SOD activities are increased, and MDA contents and NO levels are decreased compared to the model group in rats with focal cerebral ischemia/reperfusion injury. These changes may be associated with TCST.     

注射用丹参多酚酸对大鼠脑缺血再灌注线粒体ATP酶活性的影响

目的探讨注射用丹参多酚酸对大鼠脑缺血再灌注线粒体ATP酶活性的影响。方法将54只雄性SD大鼠随机分成3组(n=18):假手术组(Sham组)、缺血再灌注组(IR组)、丹参多酚酸组(Salvianolate组)。HE染色法观察大脑神经元的组织病理学变化;TTC染色检测脑梗死体积;分光光度计发法线粒体丙二醛含量和线粒体Na~+/K~+ATP酶、Ca~(2+)ATP酶、Mg~(2+)ATP酶活性。结果假手术组大鼠脑组织红染,未见梗死灶;丹参多酚酸组神经细胞变性坏死程度、脑梗死面积较缺血再灌注组明显减轻;与缺血再灌注组相比,丹参多酚酸组线粒体丙二醛含量下降(P0.05)和线粒体Na~+/K~+ATP酶、Ca~(2+)ATP酶、Mg~(2+)ATP酶活性升高(P0.05)。结论注射用丹参多酚酸对缺血再灌注损伤有保护作用,其机制与提高线粒体ATP酶活性有关。     

Discrepancy between cell injury and benzodiazepine receptor binding after transient middle cerebral artery occlusion in rats

We investigated postischemic alterations in benzodiazepine receptor, D1 dopamine receptor, and muscarinic acetylcholine receptor binding after transient middle cerebral artery (MCA) occlusion in rats using [3H]-flumazenil, [3H]-SCH23390, and [3H]-N-methyl-4-piperidyl benzilate ([3H]-NMPB), respectively, as radioligand. These ligand bindings were determined at 3 and 24 h and at 3 and 7 days after ischemia/reperfusion of MCA by using autoradiographic methods. Ischemic cell injury was clearly detected from 3 h after ischemia/reperfusion and progressively increased from 3-24 h after ischemia/reperfusion of MCA. The area of cell injury reached maximum at 24 h after ischemia/reperfusion of MCA. [3H]-SCH23390 binding was reduced to 47% of the contralateral side at 3 days after ischemia/reperfusion of MCA. After 7 days, [3H]-SCH23390 binding was further reduced by 20% in the striatum. [3H]-NMPB binding was slightly decreased in both the striatum and cerebral cortex at 3 days after ischemia/reperfusion of MCA, and [3H]-NMPB binding in the striatum and cerebral cortex were reduced to 42 and 62% of the contralateral side at 7 days after ischemia/reperfusion of MCA. [3H]-NMPB was also decreased at 24 h. In contrast, [3H]-flumazenil binding was not decreased in the striatum and cerebral cortex within 7 days after ischemia/reperfusion of MCA. These results suggest that [3H]-SCH23390 and [3H]-NMPB binding do not correlate with cell injury by ischemia/reperfusion, although vulnerability to ischemia/reperfusion was observed with these receptors. In addition, central benzodiazepine receptor imaging might be essentially stable to neuronal cell injury induced by transient focal cerebral ischemia in rats, in contrast to the results of PET studies.     

肢体缺血预处理对脑缺血再灌注损伤大鼠自噬的影响

目的探讨肢体缺血预处理对脑缺血再灌注损伤大鼠自噬的影响。方法将60只Wistar大鼠随机分为假手术组(Sham组)、缺血再灌注组(I/R组)、肢体缺血预处理组(LIPC组)、3-甲基嘌呤组(3-MA组),每组15只。制作脑缺血再灌注、肢体缺血预处理及3-MA干预大鼠模型,在脑缺血2 h再灌注24 h后进行神经功能缺陷评分和脑梗死体积测定,HE染色观察细胞形态学改变,Western Bloting法检测自噬相关蛋白Beclin-1、Cathepsin B的表达。结果与I/R组比较,LIPC组神经功能缺陷评分降低(P<0.05),脑梗体积明显减小(P<0.05),细胞损伤、坏死减轻(P<0.05),Beclin-1、Cathepsin B的蛋白表达明显减弱(P<0.05)。结论 LIPC对缺血再灌注损伤大脑具有保护作用,其机制可能与减弱自噬水平有关。     

茶氨酸对脑缺血再灌注损伤保护作用的实验研究

目的观察茶氨酸对脑缺血再灌注损伤的保护作用,为临床脑缺血再灌注损伤的预防和治疗提供实验依据。方法将24只健康家兔随机分为四组：假手术组、脑缺血组、茶氨酸予处理组和茶氨酸治疗组。麻醉后分离血管,采用基底动脉、双侧颈总动脉结扎法制备急性全脑缺血再灌注动物模型。假手术组仅分离动脉不结扎,予处理组在缺血前应用茶氨酸,治疗组在缺血后应用茶氨酸,缺血组不作特殊药物处理。各组分别在规定时间点即缺血前、再灌注后30min、1h、2h采血测定神经特异性烯醇化酶(NSE)含量,取脑组织活检观察超微结构,处死动物测定脑含水量。结果茶氨酸予处理组和治疗组以上各项指标均较脑缺血组有显著的改善,提示茶氨酸具有神经保护作用。实验还显示茶氨酸予处理组在再灌注30min时NSE含量与假手术组比较无差异,提示用茶氨酸予处理后可能使缺血后脑损害的发生延迟,为进一步的治疗争取了宝贵时间。结论茶氨酸对脑缺血再灌注损伤有保护作用,值得进一步研究。     

尼莫地平对大鼠急性脑缺血再灌注损伤早期保护作用的研究

目的探讨尼莫地平对急性脑缺血再灌注损伤的早期保护作用。方法线栓法复制大鼠急性脑缺血模型。30只雄性Wistar大鼠随机分为假手术、模型、尼莫地平3组。模型组采取缺血2h再灌注2h。尼莫地平组大鼠在缺血0时刻起每小时腹腔注射给药一次,剂量为5mg/kg。各组大鼠在手术4h后实验结束后,行腹主动脉采血,同时取完整脑组织。脑组织切片进行TTC染色,并比较各组脑组织梗死面积。检测各组大鼠血清及脑组织匀浆中SOD、MDA、NO含量。结果与模型组相比,尼莫地平组大鼠脑组织梗死面积显著减少。血清生化指标显示,模型组SOD含量显著低于假手术组,给予尼莫地平治疗后,SOD含量增加明显。模型组MDA、NO含量明显高于假手术组,尼莫地平组明显降低血清中MDA、NO。结论尼莫地平对大鼠急性脑缺血再灌注损伤有保护作用,这种保护作用与NO和氧化应激密切相关。     

In vivo measurement of cytosolic free calcium during cerebral ischemia and reperfusion

An increase in cytosolic free calcium concentration ([Ca2+]i) may trigger irreversible cell injury following cerebral ischemia. We have measured changes in [Ca2+]i in cat cortex in vivo during ischemia produced by 1 hour of middle cerebral artery occlusion and during 30 minutes of reperfusion. Indo-1, a fluorescent Ca2+ indicator, was loaded into the exposed cortex by superfusion, and changes in the [Ca2+]i signal (400/506 nm ratio) were measured microfluorometrically during ultraviolet excitation (340 nm). The nicotinamide adenine dinucleotide/reduced nicotinamide adenine dinucleotide (NAD/NADH) redox state and hemodynamic changes were measured simultaneously. The animals showing severe deterioration in their electroencephalograms (EEG) showed a progressive increase in the [Ca2+]i signal during ischemia (baseline: 1.46 +/- 0.05; 60 minutes after occlusion: 2.99 +/- 0.37; n = 7). At 30 minutes following reperfusion, the animals showing little recovery in their EEG exhibited a further increase in [Ca2+]i (4.71 +/- 0.87, n = 3), whereas animals showing significant recovery in their EEG also showed recovery of [Ca2+]i (1.55 +/- 0.09, n = 4). By contrast, the moderate or mild stroke animals with less deterioration in their EEGs showed no increase in [Ca2+]i during either ischemia or reperfusion. These data suggest that the increase in [Ca2+]i might be closely related not only to deterioration of brain function during ischemia but also to poor recovery during the reperfusion period.     

缺血后处理对局灶脑缺血再灌注大鼠Toll样受体2表达的影响

目的 探讨缺血后处理对大鼠局灶性脑缺血再灌注时Toll样受体2(TLR2)表达的影响。方法 成年雄性SD大鼠90只,分为假手术组、缺血再灌注组、缺血后处理组各30只; 用线栓法建立局灶性大脑中动脉闭塞模型(MCAO),随机分为假手术组(sham)、缺血再灌注组(I/R)、缺血后处理组(IPC),分别于再灌注24、48、72 h后留取大脑皮质组织; 采用Longa的等级评分法进行神经行为学评分,免疫组化和蛋白质印记(Western blot)法检测TLR2蛋白的表达水平,逆转录-聚合酶链反应(RT-PCR)检测TLR2 mRNA表达水平。结果(1)缺血后处理组大鼠神经行为学评分明显改善;(2)缺血再灌注组TLR2蛋白在再灌注24、48、72 h表达水平明显升高(P<0.05); 缺血后处理组TLR2蛋白表达在各时间点均减少(P<0.05); TLR2 mRNA的表达趋势与蛋白表达基本一致。结论 缺血后处理可以降低TLR2表达水平,这可能是其脑保护作用的部分机制之一。     

Dose-dependent effects of procyanidin on nerve growth factor expression following cerebral ischemia/ reperfusion injury in rats★

BACKGROUND： Recently, grape seed procyanidin （GSP） has been shown to be exhibit antioxidant effects, effectively reducing ischemia/reperfusion injury and inhibiting brain cell apoptosis. OBJECTIVE： To study the effects of GSP on nerve growth factor （NGF） expression and neurological function following cerebral ischemia/reperfusion injury in rats. DESIGN： Randomized controlled study based on SD rats. SETTING： Weifang Municipal People＇s Hospital. MATERIALS： Forty-eight healthy adult SD rats weighing 280-330 g and irrespective of gender were provided by the Experimental Animal Center of Shandong University. GSP derived from grape seed was a new high-effective antioxidant provided by Tianjin Jianfeng Natural Product Researching Company （batch number： 20060107）. Rabbit-anti-rat NGF monoclonal antibody was provided by Beijing Zhongshan Biotechnology Co., Ltd., and SABC immunohistochemical staining kit by Wuhan Boster Bioengineering Co., Ltd. METHODS： The present study was performed in the Functional Laboratory of Weifang Medical College from April 2006 to January 2007. Forty-eight SD rats were randomly divided into the sham operation group, ischemia/reperfusion group, high-dose GSP （40 mg/kg） group, or low-dose GSP （10 mg/kg） group （n = 12 per group）. Ischemia/reperfusion injury was established using the threading embolism method of the middle cerebral artery. Rats in the ischemia/reperfusion model group were given saline injection （2 mL/kg i.p.） once daily for seven days pre-ischemia/reperfusion, and once more at 15 minutes before reperfusion. Rats in the high-dose and low-dose GSP groups were injected with GSP （20 or 5 mg/mL i.p., respectively, 2 mL/kg） with the same regime as the ischemia/reperfusion model group. The surgical procedures in the sham operation group were as the same as those in the ischemia/reperfusion model group, but the thread was approximately 10 mm long, thus, the middle cerebral artery was not blocked. MAIN OUTCOME MEASURES： NGF expression in the     

脑缺血再灌流［~3H］—三磷酸肌醇放射活性及突触体游离Ca~（2＋）的变化

本文研究了大鼠脑缺血再灌流时［３Ｈ］—三磷酸肌醇（［３Ｈ］－ＩＰ３）放射活性及突触体游离Ｃａ２＋（［Ｃａ２＋］ｉ）的变化，并用苯甲基磺酰氟化物（ＰＭＳＦ）治疗，观察其对［３Ｈ］－ＩＰ３放射活性及突触体［Ｃａ２＋］ｉ的影响。结果：脑缺血１ｍｉｎ［３Ｈ］－ＩＰ３放射活性非常显著地增高。缺血２０ｍｉｎ、缺血２０ｍｉｎ再灌流１ｈ、６ｈ、２ｄ［３Ｈ］－ＩＰ３放射活性非常显著地降低。缺血２０ｍｉｎ突触体［Ｃａ２＋］ｉ非常显著地增高，至再灌流６ｈ达到最高水平。应用ＰＭＳＦ治疗能显著地抑制突触体［Ｃａ２＋］ｉ的升高。     

Monosialotetrahexosy-1 ganglioside attenuates diabetes-associated cerebral ischemia/reperfusion injury through suppression of the endoplasmic reticulum stress-induced apoptosis

We aimed to assess the neuroprotective mechanism of monosialotetrahexosy-1 ganglioside (GM1) on focal cerebral ischemia/reperfusion (I/R) injury in rats with diabetes. A total of 54 male Wistar rats were induced with diabetes mellitus by administration of streptozotocin (STZ). The rats were then randomized into three groups, including sham group (n = 18), I/R group (n = 18), and GM1 group (n = 18). Focal cerebral ischemia was modeled using the right middle cerebral artery occlusion method. In the GM1 group, diabetic rats were intraperitoneally administered with GM1 (15 mg/kg) at 20 min prior to reperfusion. GM1 was replaced by an equal volume of saline in the I/R group. Rats from the sham group accepted sham operation and normal saline. The neurological deficit and brain infarct volume and TUNEL-apoptosis were evaluated. The expression of endoplasmic reticulum (ER) stress-related proteins, including caspase-12, GRP78 and CHOP/GADD153, was examined by Western blot. GM1 notably reduced the cerebral infarct size and improved the neurological behavior. In addition, GM1 dramatically reduced TUNEL-positive cell numbers in the cerebral cortex. Furthermore, GM1 treatment modulated protein levels, increasing GRP78 and reducing CHOP/GADD153 expression along with activation of caspase-12 in the ischemic brain hemispheres. These results imply that GM1 attenuates diabetes-associated cerebral I/R injury by suppressing the ER stress-induced apoptosis.     

γ-氨基丁酸转运体-1与局灶性脑缺血再灌注神经元损伤关系的实验研究

目的探讨γ氨基丁酸转运体1(GAT1)与脑缺血再灌注神经元损伤的关系。方法制备大鼠局灶性脑缺血再灌注模型,分别在脑缺血再灌注3h、6h、12h、24h及3d取损伤侧脑组织进行免疫组化染色,测定标本中GAT1阳性神经元数目和光密度值,并与正常组和假手术组比较。结果脑缺血再灌注3hGAT1表达明显上调(P<0.05),6h达到高峰(P<0.01),12h开始下降,24h后与对照组比较差异无显著性。结论脑缺血再灌注早期GAT1阳性神经元明显增多,其在局灶性脑缺血再灌注中可能参与神经元损伤病理生理过程。     

丁苯酞预处理对大鼠脑缺血再灌注损伤的神经保护作用

目的研究丁苯酞预处理对大鼠局灶性脑缺血再灌注损伤的神经保护作用。方法健康成年SD雄性大鼠48只,随机分为假手术组、缺血再灌注组、丁苯酞预处理组,每组各16只。各组均灌胃5d后,采用线栓法制作大鼠局灶性脑缺血再灌注(MCAO)模型,缺血2h、再灌注24h,进行神经功能缺损评分,TTC染色及图像分析观察脑梗死体积,免疫组化法检测脑组织caspase-3、bcl-2表达的变化。结果与缺血再灌注组相比,丁苯酞预处理组神经缺损程度改善,梗死灶体积减少,caspase-3阳性细胞数量减少,bcl-2表达上调。结论丁苯酞可减轻缺血性脑血管病的发作,具有一定的神经保护作用。     

氯喹对大鼠全脑缺血/再灌注后学习能力的影响

目的观察氯喹对大鼠全脑缺血/再灌注后的学习能力的影响。方法采用Pulsinelli-Brierley 4动脉阻断方法制作大鼠全脑缺血/再灌注损伤模型,使用HE染色方法观察各组大鼠海马区的损伤情况,用Y型电迷宫检测各组大鼠的学习记忆能力。结果氯喹处理组大鼠海马区损伤较缺血损伤组大鼠减轻,氯喹处理组大鼠学习记忆能力强于缺血损伤组大鼠,但仍比假手术组大鼠差（P〈0.05）。结论氯喹可以通过减轻大鼠全脑缺血后海马损伤减轻学习记忆能力的损伤。     

复方甘草酸苷对兔骨骼肌缺血再灌注损伤的影响*

背景：甘草酸苷对缺血再灌注损伤保护作用的研究主要集中于心、肾、肠等器官,对骨骼肌的研究甚少。 目的：验证复方甘草酸苷对兔骨骼肌缺血再灌注损伤的保护作用。 设计、时间及地点：血清学及组织形态学水平的随机对照动物实验,于2008-02/09在重庆医科大学临床检验诊断学教育部重点实验室完成。 材料：选用24只新西兰大白兔,按随机数字表法分为3组,即假手术组、模型组及复方甘草酸苷组,每组8只。 方法：模型组动物制备右后肢骨骼肌缺血损伤模型,缺血4 h后再灌注24 h;复方甘草酸苷组动物缺血4 h后给予复方甘草酸苷20 mg/kg,再灌注24 h;假手术组动物仅游离出股动脉不进行缺血,4 h后缝合切口并给予等量生理盐水。 主要观察指标：观察肌肉损伤后甘草酸苷对血浆乳酸脱氢酶、肌酸激酶活性及丙二醛浓度,肌组织髓过氧化物酶活性、湿质量/干质量比值及P-选择素mRNA表达水平的影响;光镜下观察骨骼肌的组织形态学改变。 结果：假手术组的血浆肌酸激酶、乳酸脱氢酶活性和丙二醛浓度显著低于缺血再灌注组及复方甘草酸苷组(P < 0.05),复方甘草酸苷组显著低于缺血再灌注组(P < 0.01)。假手术组的骨骼肌组织髓过氧化物酶活性和湿质量/干质量比值显著低于缺血再灌注组及复方甘草酸苷组(P < 0.01),复方甘草酸苷组显著低于缺血再灌注组(P < 0.01)。10倍镜下坏死肌纤维数缺血再灌注损伤组显著大于复方甘草酸苷组(P < 0.05)。骨骼肌组织中P-选择素 mRNA 表达水平假手术组显著低于缺血再灌注组(P < 0.01),复方甘草酸苷组显著低于缺血再灌注组(P < 0.05)。 结论：复方甘草酸苷对骨骼肌缺血再灌注损伤有明显的保护作用。