大鼠脑梗死后神经前体细胞移行及电针作用的研究

目的研究成年大鼠脑梗死后电针作用对内源性神经前体细胞移行的影响。方法采用易卒中型肾性高血压大鼠（RHRSP）,电凝法凝闭大脑中动脉（MCAO）。用Garcia评分、HE染色、免疫荧光等方法观察电针对脑梗死后1周、2周、3周、4周大鼠脑内梗死灶体积,行为学评分及5-溴脱氧尿核苷（Bromodeoxyuridine,Brdu）、Doublecortin（DCX）阳性细胞数的干预作用,并与脑梗死组和对照组比较。结果电针治疗后前3周梗死体积较脑梗死组缩小（P〈0.05）;电针后2d与3d大鼠行为学评分较梗死组高（P〈0.05）;MCAO后梗死灶边缘有Brdu阳性细胞和DCX阳性细胞分布。电针组Brdu阳性细胞较脑梗死组明显增加（P〈0.05）,电针组DCX阳性细胞数在1周末明显高于脑梗死组（P〈0.05）。结论电针促进神经功能恢复,减小脑梗死体积,并使缺血灶周移行的神经前体细胞增多,可能与其改变脑内微环境密切相关。     

Effects of acupuncture plus mild hypothermia on apoptosis-related factors in rats with cerebral ischemia-reperfusion

Objective

To investigate the effect of acupuncture plus mild hypothermia on neurological function impairment score, cerebral infarct size and apoptosis-related factors in cerebral ischemia reperfusion injury (CIRI) rats.

Methods

Sixty healthy male Sprague-Dawley (SD) rats were routinely reared for 1 week. Ten rats were randomly selected as the sham operation group and 10 rats as the blank control group, while the remaining 40 rats were subjected to preparing the middle cerebral artery occlusion (MCAO) model by modified filament occlusion method. The 40 MCAO rats were further randomly divided into a model group, an acupuncture group, a mild hypothermia group and an acupuncture plus mild hypothermia group, with 10 rats in each group. Rats in the sham operation group, the blank control group and the model group did not accept treatment except binding; rats in the acupuncture group received acupuncture treatment; rats in the mild hypothermia group received mild hypothermia treatment; rats in the acupuncture plus mild hypothermia group received acupuncture and mild hypothermia treatment. 72 h after the treatment, neurological function impairment score was performed; the infarct area ratio was determined by 2,3,5-tripheyl tetrazolium chloride (TTC) staining; apoptosis of brain cells was observed by TUNEL method; the expressions of Bcl-2, Bax and Caspase-3 were detected by immunohistochemistry.

Results

Compared with the blank control group and the sham operation group, the neurological function impairment score, cerebral infarct area ratio, apoptosis, and the expressions of Bax and Caspase-3 in the model group were significantly increased, while the expression of Bcl-2 was significantly decreased, and there were significant between-group differences (all P<0.05). After the treatment, there were statistically significant differences among the treatment groups in the neurological function impairment score, cerebral infarct area ratio and apoptosis in the ischemic side of rats, as well as the expressions of Bcl-2, Bax and Caspase-3 (all P<0.05), and from the figures, tables and statistical analysis, it was found that a better tendency in the acupuncture plus mild hypothermia group than the acupuncture group or mild hypothermia group.

Conclusion

Acupuncture plus mild hypothermia can protect the brain cells by improving neurological function impairment, decreasing cerebral infarct area ratio, reducing the number of apoptotic cells in the ischemic area and regulating the expressions of apoptosis related proteins to inhibit apoptosis.

     

Effect of Ginkgo biloba leaf extract on cerebral cortex amino acid levels in cerebral ischemia model rats

OBJECTIVE: To investigate the effect of Ginkgo biloba leaf extract on amino acid levels in the cerebral cortex of cerebral ischemia model rats induced by middle cerebral artery occlusion(MCAO).METHODS: A rat model of cerebral ischemia was established by MCAO. Male rats were divided into a negative control group(Control), a sham-operated group(Sham), an ischemic group(MCAO), and an ischemic group treated with Ginkgo biloba leaf extract(MCAO_D). All groups were divided into two subgroups with occlusion times of 12 and 24 h, respectively. The levels of 18 endogenous amino acids in the cerebral cortex were quantified by triple quadrupole-liquid chromatography-mass spectrometry.RESULTS: Compared with the MCAO group, behavioral performance, neurological deficit score, and cerebral infarct volume were significantly improved in the MCAO_D group(P 0.05, P 0.01). Compared with the sham group, the levels of 17 amino acids in the cerebral cortex were markedly changed in the MCAO group. The levels of Alanine(Ala), Isoleucine(Ile), Glutamic acid(Glu), Serine(Ser), Valine(Val), Phenylalanine(Phe), Proline(Pro),Threonine(Thr), Lysine(Lys), Tyrosine(Tyr), Hydroxyproline(Hyp), Arginine(Arg), Leucine(Leu),Tryptophan(Trp), and Glycine(Gly) were increased(P 0.001, P 0.05), while levels of Gln and Tau were decreased(P 0.001, P 0.05). Compared with the MCAO group, Ginkgo biloba extract treatment in the MCAO_D group significantly down-regulated the levels of 11 amino acids, especially those of Arg, Thr, and Ser in 12 or 24 h.CONCLUSION: Injection of Ginkgo biloba leaf extract has a therapeutic effect on model rats with MCAO-induced cerebral ischemia by acting on amino acids in the cerebral cortex. This effect might be associated with the regulation of amino acid metabolism in the cerebral cortex.     

三七二醇预处理诱导脑缺血耐受及对GFAP表达的影响

目的:观察三七二醇皂甙(PDS)预处理诱导脑缺血耐受及对胶质纤维酸性蛋白(GFAP)表达水平的影响。方法:SD雄性健康大鼠120只,随机分为6组。空白组未行任何干预;模型组(MCAO组)采用longa氏二次线栓法;预缺血 模型组(IPC MCAO组)先预缺血10 min,3 d后行MCAO术2 h;三七二醇预处理组(PDS MCAO组)予腹腔注射PDS 50 mg/kg.d,3 d后行MCAO术2 h;三七二醇治疗组(MCAO PDS组)予MCAO术后2 h腹腔注射PDS 50 mg/kg.d,3 d后处死;假手术组(SS SS组)间隔3 d分别施以10 min和2 h假手术。比较各组神经功能缺损评分、脑梗死体积及GFAP的表达水平。结果:IPC MCAO组、PDS MCAO组脑梗死体积较MCAO组缩小,GFAP表达水平较MCAO组升高,有统计学差异(P<0.05)。结论:PDS预处理诱导了脑缺血耐受,对将要发生的严重脑缺血具有保护作用。星形胶质细胞的活化可能是三七二醇预处理诱导脑缺血耐受的重要机制。     

苦碟子注射液对缺血性脑卒中火毒证大鼠作用的差异蛋白质研究

探讨中药苦碟子注射液对缺血性脑卒中火毒证大鼠脑组织蛋白质表达的调控作用。采用角叉菜胶复合大脑中动脉阻塞（MCAO）方法制备缺血性脑卒中火毒证大鼠模型,按随机数字表法将SD大鼠分为药物组、模型组和假手术组。采用TTC染色法和HE染色法对脑组织进行大体观察和病理形态学观察;利用双向凝胶电泳技术寻找缺血性脑卒中火毒证大鼠和假手术大鼠之间与疾病相关的差异表达蛋白,并观察应用苦碟子注射液连续干预72 h后,对差异蛋白表达水平的影响。结果显示,缺血性脑卒中火毒证大鼠与假手术大鼠间有差异表达蛋白,连续给予具有清热解毒通络作用的苦碟子注射液能够减轻脑组织缺血形态学改变,调节部分差异蛋白表达水平。     

复健片对大脑中动脉闭塞模型大鼠未损伤侧脑组织GAP-43表达的影响

目的:观察复健片对大脑中动脉闭塞(MCAO)模型大鼠未损伤侧大脑皮质生长相关蛋白43(GAP-43)表达的影响,探讨复健片促进未损伤侧大脑重塑的分子基础。方法:110只SD雄性大鼠,按随机数字表法随机分为假手术组20只和造模组90只。根据处死时间点及干预方法不同,假手术组及模型组各分为术后1周、2周、3周、4周和5周五个亚组,药物组分为术后2周、3周、4周和5周四个亚组。造模组采用线栓法制备大鼠右侧大脑中动脉永久性闭塞(MCAO)模型,药物组术后1周末按5.9 m L/kg给予复健片浓缩液灌胃,采用横木行走实验(BWT)评定各组大鼠运动功能;TTC染色观察梗死灶部位;采用Western blot法检测大鼠左侧大脑GAP-43的表达。结果:术后1周末,模型组较假手术组GAP-43表达增高;术后2周末,模型组和药物组GAP-43表达均较假手术组增高,其中药物组增高更为显著;术后3周、4周末延续术后2周末的趋势;术后5周,药物组仍高于模型组,模型组与假手术组已无显著差异。与此同时,BWT评分结果示,模型组药物组BWT评分在术后1、2、3、4周末均升高(P0.01),其中药物组的升高更显著,直至术后5周末,药物组与假手术组已无明显差异(P0.05)。TTC染色表明术后5周末MCAO大鼠梗死灶体积无差异。结论:复健片通过增加MCAO模型大鼠健侧大脑GAP-43表达,从而促进神经突起生长,继而促进未损伤侧大脑重塑以改善大鼠缺血性脑卒中后的运动功能恢复。     

Huang-Lian-Jie-Du-Decotion induced protective autophagy against the injury of cerebral ischemia/reperfusion via MAPK-mTOR signaling pathway

Ethnopharmacological relevance

Huang-Lian-Jie-Du-Decotion (HLJDD, Hwangryun-Hae-Dok-Decotion in Japan), an ancient antipyretic and detoxifying traditional Chinese medicine formula, was reported to have protective effect on ischemic stroke.

Aim of the research

To investigate the therapeutic effect of HLJDD on ischemic stroke and explore its mode of action.

Material and methods

A model of ischemic stroke in the rat was established after transient middle cerebral artery occlusion (MCAO) followed by reperfusion. Rats were assigned randomly to groups of control, sham, transient ischemia/reperfusion (I/R), and three treatment groups by HLJDD at 2.5, 5.0, 10.0 mg/kg. The neurological deficit, the cerebral infarct size, morphology abnormality, biochemical parameters were examined, and the levels of relevant proteins were determined by immunoblotting analysis to evaluate the protective effects of HLJDD on ischemic stroke and explore the underlying mechanism.

Results

Compared with I/R group, HLJDD significantly ameliorated neurological deficit and histopathology changes, decreased infarct area, and restored the levels of biochemical indicators including nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH), glutathione disulfide (GSSG), total superoxide dismutase (T-SOD), Cu/Zn-SOD, Mn-SOD and glutathione peroxidase (GSH-PX). HLJDD also notably elevated the levels of microtubule-associated protein1 light chain 3 (LC3), Beclin-1, and other autophagy related genes (Atgs), promoted the activation of extracellular signal-regulated kinases (ERK), protein kinase B (Akt), 3-phosphoinositide-dependent kinase (PDK1), and inhibited the activation of mammalian target of rapamycin (mTOR), c-Jun N-terminal protein kinases (JNK), p38, phosphatase and tensin homolog (PTEN).

Conclusion

HLJDD showed neuroprotective effects on ischemic stroke, at least in part to the induced protective autophagy via the regulation of mitogen-activated protein kinase (MAPK) signals. This Akt-independent protective autophagy is favorable in the treatment of stroke, avoiding unfavorable side-effects associated with the inactivation of Akt. The efficacy of HLJDD on ischemic stroke and its safety warranted by its long-term clinical use in traditional Chinese medicine favored further study to develop HLJDD as an effective therapeutic agent to treat ischemic stroke.     

银杏二萜内酯葡胺注射液对大鼠局灶性脑缺血的保护作用

探讨银杏二萜内酯葡胺注射液对大鼠局灶性脑缺血再灌注损伤(MCAO)的保护作用,并探讨其可能的作用机制。雄性SD大鼠140只,随机分为假手术组、模型组、银杏提取物注射液(金纳多,1.0 m L·kg~(-1))、尼莫地平注射液(0.2 mg·kg~(-1))组、银杏二萜内酯葡胺注射液(5.2,2.6,1.3 mg·kg~(-1))组;所有动物手术前4 d尾静脉注射给药(模型组及假手术组给予生理盐水)。除假手术组,其他动物通过右侧大脑中动脉线栓塞法(MCAO)制作局灶性脑缺血再灌注模型。缺血3 h后,所用动物再次尾静脉注射给药。大鼠缺血再灌注后进行神经行为学评分并采用TTC染色法观察脑组织梗死率;测定脑组织匀浆中超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、丙二醛(MDA)、乳酸(LA)含量及脑脊液中Ca~(2+),谷氨酸(Glu),天冬氨酸(Asp)以及磷酸肌酸激酶(CK-BB)和乳酸脱氢酶(LDH)含量的变化。与假手术组相比,模型组大鼠脑梗死率显著增加,神经严重缺损;脑组织匀浆中MDA、LA含量升高,GSH、SOD含量降低;脑脊液中Ca~(2+)浓度降低,Glu和Asp的含量及CK-BB、LDH含量显著升高。与模型组相比,银杏二萜内酯葡胺注射液高、中剂量组能显著减少脑梗死率,改善脑神经功能缺损症状;提高SOD、GSH活性,减少血清中MDA、LA含量;升高脑脊液中Ca~(2+)浓度,减低神经递质Glu和Asp的含量及CK-BB、LDH的含量。银杏二萜内酯葡胺注射液能明显改善模型动物的神经功能缺损,其机制可能与修复血脑屏障,减少自由基,减少细胞外游离钙内流,降低脑脊液中兴奋性氨基酸含量等有关,从而保护脑缺血。     

安宫牛黄丸（含天然麝香或人工麝香）对实验性脑缺血的保护作用

目的:研究比较含人工麝香或天然麝香的安宫牛黄丸对实验性脑缺血的保护作用.方法:采用大脑中动脉栓塞(MCAT)与大脑中动脉缺血再灌注(MCAO)两种动物模型,观察两种安宫牛黄丸(84～333 mg· kg-1)对大鼠的神经症状、脑梗死范围以及对缺血侧脑组织酸中毒和自由基代谢的影响.结果:安宫牛黄丸(含人工麝香或天然麝香)167,333 mg· kg-1剂量组可显著改善MCAT大鼠的神经症状;安宫牛黄丸(含天然麝香)84,167 mg· kg-1剂量组可分别减少MCAT大鼠脑梗死范围27％和37％,安宫牛黄丸(含人工麝香)84～333 mg·kg-1显著减少MCAT大鼠脑梗死灶面积21％～32％,两种安宫牛黄丸对应各剂量组间无显著性差异;两者均可显著降低MCAO大鼠的LDH(10％～12％)和MDA(28％～38％)含量,并显著升高SOD活力(15％～36％)和GSH含量(14％～36％).结论:含人工麝香或天然麝香的安宫牛黄丸均可通过改善氧化应激损伤而对实验性脑缺血有保护作用,且二者作用未见显著差异.     

蒙医温针对局灶性脑缺血早期脑组织VEGF含量和脑水肿的影响

目的:探讨蒙医温针对大鼠局灶性脑缺血再灌注后脑组织VEGF水平、脑梗死体积,脑含水量的影响。方法:将雄性SD大鼠随机分为蒙医温针组、针刺组、尼莫地平组、假手术组、模型组5组。采用改良线栓法建立大鼠中动脉阻塞再灌注模型,各组在造模成功1 h时进行治疗,1次/d,假手术组和模型组不给于治疗。各组大鼠在术后24 h进行神经功能评分及测脑组织VEGF水平和脑梗死体积及脑含水量。结果:假手术组无神经功能缺损症状,蒙医温针组与各组比较脑组织VEGF含量有统计学意义,各组脑梗死体积、脑含水量与假手术组比较均有统计学意义,蒙医温针组脑梗死体积、脑含水量与模型组比较有统计学意义。结论:蒙医温针有改善大鼠局灶性脑梗死后的神经功能和减轻脑水肿、降低脑梗死体积作用。蒙医温针治疗缺血性脑卒中进行早期干预具有十分重要的临床意义。     

丹参酮预处理诱导内源性神经保护及对热休克蛋白70表达的影响

目的探讨丹参酮预处理对局灶脑缺血热休克蛋白70（HSP70）表达的影响及丹参酮预处理诱导内源性神经保护及其机制。方法SD大鼠随机分为大脑中动脉闭塞（MCAO）组、预缺血组、丹参酮预处理组、空白对照组，利用二次线栓法制备大脑中动脉闭塞模型。采用TTC染色及免疫组化法，比较各组梗死体积和HSP70的表达。结果丹参酮预处理组和预缺血组梗死体积较MCAO组明显减少；HSP70表达明显高于MCAO组及空白对照组。结论丹参酮预处理可以诱导内源性神经保护，增高HSP70表达可能是内源性神经保护机制之一。     

肉苁蓉总苷对大鼠局灶性脑缺血损伤的影响

目的研究肉苁蓉总苷(GCs)对大鼠局灶性脑缺血损伤的保护作用。方法采用插线法阻塞大鼠大脑中动脉(MCAO)制造大鼠局灶性脑缺血模型，采用NBT染色测定脑梗死范围．用“重量求面积法”计算梗死组织占对侧大脑质量的百分比作为对梗死范围的判定．行为指标评分采用11分评分制，并测定缺血脑组织的抗氧化酶活性及丙二醛(MDA)含量。结果GCs125，250mg／kg可明显缩小脑梗死范围，改善神经症状，脑组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性明显升高，MDA含量显著下降。结论GCs对大鼠局灶性脑缺血损伤具有神经保护作用，此作用可能与SOD，GSFH-Px活性水平的升高有关。     

回春偏瘫方对缺血再灌注大鼠脑神经生长因子及脑源性神经营养因子表达的影响

目的:建立缺血性中风后动物模型,探讨回春偏瘫方对缺血性中风模型动物脑内神经生长因子(NGF)及脑源性神经营养因子(BDNF)水平的影响。方法:用线栓法造成大脑中动脉阻塞(MCAO)再灌注模型,造模成功后随机分为假手术组,模型组,回春偏瘫方高、中、低剂量,西药尼莫地平组(西药组),连续给药14天,然后取材,用酶联免疫吸附法测定缺血再灌注大鼠颅内NGF水平、免疫组化染色观察脑源性神经营养因子(BDNF)在颅内的表达。结果:治疗组动物脑内NGF、BDNF水平均高于模型组(P<0.05),尤以中剂量组效果最佳。结论:回春偏瘫方可增加模型动物脑内NGF、BDNF水平,这可能是回春偏瘫方治疗缺血性中风机制之一。     

丹参酚酸A对脑缺血大鼠神经功能及热休克蛋白基因表达的影响

目的:探讨丹参酚酸A对脑缺血大鼠神经功能及热休克蛋白基因表达的影响,为其脑保护机制研究提供参考。方法:选用80只健康成年雄性SD大鼠作为研究对象,通过线栓法对动脉缺血再灌注损伤模型进行制备,并采用随机数字表法将其分为假手术组、模型组、低剂量组和高剂量组,每组各20只。比较各组大鼠实验后24 h脑梗死体积和实验72 h后胶质源性神经营养因子(GDNF)、脑源性神经营养因子(BDNF)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化物歧化酶(SOD)水平,分析实验24、48、72 h后神经行为学评分变化。在再灌注24、48、72 h后取大鼠脑组织,采用免疫组织化学染色和原位杂交法对大鼠脑组织HSP70蛋白和HSP70 mRNA水平进行测定。结果:低剂量组、高剂量组大鼠脑梗死面积均低于模型组,且高剂量组脑梗死体积明显更低。实验24、48、72 h后,低剂量组、高剂量组大鼠神经行为学评分均低于模型组,且高剂量组神经行为学评分明显更低。模型组、低剂量组、高剂量组大鼠脑组织BDNF、GDNF、MDA水平均明显高于假手术组,SOD、GSH-Px水平明显低于假手术组; 且模型组、低剂量组、高剂量组脑组织大鼠BDNF、GDNF、SOD、GSH-Px水平呈现升高的趋势,MDA水平呈现降低趋势。实验24、48、72 h后,模型组、低剂量组、高剂量组大鼠缺血皮层内HSP70 mRNA阳性细胞计数、HSP70蛋白表达OD值均明显高于假手术组,且模型组、低剂量组、高剂量组缺血皮层内HSP70 mRNA阳性细胞计数、HSP70蛋白表达OD值呈现升高的趋势,差异具有统计学意义(P<0.05)。结论:丹参酚酸A可以有效地对脑缺血再灌注损伤大鼠的自由基进行清除,减少梗死面积,增加HSP70蛋白基因的表达,具有较好的缺血脑保护作用。     

电针刺激“足三里”和“内关”对脑梗塞大鼠GAP-43表达的影响

目的：探讨电针刺激“足三里”和“内关”对脑梗塞大鼠梗死区周围神经生长相关蛋白43（GAP-43）表达情况的影响，从而进一步揭示电针对脑梗塞大鼠脑神经可塑性的影响及其机制。方法：将60只大鼠，随机分为假手术组，针刺组和非针刺组,每组大鼠再随机分为1d、7d和14d共9个亚组；用线栓法制备脑梗塞模型；针刺组大鼠进行电针刺激“足三里”和“内关”治疗,20min/次/天；非针刺组和假手术组在相同时间予以捆绑固定，不进行针刺治疗。采用NSS评分来评价神经功能缺损情况、免疫组化法测定各组大鼠脑梗死区周围GAP-43表达的变化情况。结果： 1d时大鼠脑组织梗死区周围GAP-43的表达3组之间没有明显差别(P>0.05)；7d和14d时针刺组均明显高于假手术组和非针刺组(P<0.01)。结论：电针刺激“足三里”和“内关”能够改善脑脑梗塞大鼠神经功能，促进其神经功能重塑，其机制可能与增加脑梗塞大鼠脑梗死区GAP-43表达水平有关。     

银杏二萜内酯葡胺注射液对大鼠急性脑缺血再灌注损伤的影响

目的:探讨银杏二萜内酯葡胺注射液对线栓法致大鼠急性脑缺血再灌注损伤(MCAO)的保护作用,并探讨其可能的作用机制。方法:雄性SD大鼠96只,随机分为假手术组、模型组、尼莫地平(0.4 mg·kg-1)组、银杏二萜内酯葡胺注射液高、中、低(4.8,2.4,1.2 g·kg-1)剂量组。所有动物手术前2 d尾静脉注射给药(模型组及假手术组给予生理盐水)。除假手术组,其他动物通过右侧大脑中动脉线栓塞法(MCAO)制作局灶性脑缺血再灌注模型。缺血3 h后,所用动物再次尾静脉注射给药。采用脑组织TTC染色法观察梗死率;放免法测定血清中磷酸肌酸激酶脑型同工酶(CK-BB)、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量;免疫组化法测定脑组织中半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)表达。结果:与正常组比较,模型组大鼠脑梗死率显著增加,神经缺损症状严重;血清中SOD活性降低,MDA,CK-BB含量显著增加;脑组织中Caspase-3表达量显著升高。与模型组比较银杏二萜内酯葡胺注射液中剂量组能显著减少脑梗死率,改善脑神经功能缺损症状;提高SOD活性,减少血清中MDA,CK-BB含量,抑制脑组织中Caspase-3表达。结论:银杏二萜内酯葡胺注射液对大鼠局灶性脑缺血再灌注损伤具有保护作用,作用机制可能与其修复血脑屏障、降低血清CK-BB含量、抗自由基损伤及抑制Caspase-3表达有关。     

滋肾通络方对MCAO大鼠代谢性谷氨酸受体1α基因表达的影响

目的：观察滋肾络通络方对MCAO大鼠脑组织代谢性谷氨酸受体1α（mGluR1α）基因表达的变化,以探讨mGluR1α在脑缺血中的意义及滋肾通络方对其影响。方法：制作ΜCAO大鼠模型,随机分为假手术组、模型组、中药高剂量组、中药低剂量组和西药组。灌胃20天后,取大鼠脑组织,用免疫组织化学、逆转录-聚合酶链反应（RT-PCR）技术和HE染色检测各组mGluR1α的蛋白表达、mRNA转录水平及坏死神经元的计数。结果：各缺血组mGluR1α表达均高于假手术组,药物治疗组mGluR1α的mRNA转录均低于模型组,且中药高剂量组mGluR1α蛋白表达低于西药组。结论：脑缺血可引起mGluR1α表达上调,提示mGluR1α参与介导了局灶性脑缺血损伤。滋肾通络方可降低mGluR1α的蛋白表达,从而对脑缺血损伤具有保护作用。     

羚蝎胶囊对局灶性脑缺血再灌注模型大鼠脑组织超氧化物歧化酶和丙二醛的影响

目的探讨羚蝎胶囊治疗缺血性中风的作用机制。方法将30只SD大鼠随机分为假手术组、模型组、羚蝎胶囊组。采用穿线法阻断大脑中动脉（MCAO）复制大鼠脑缺血再灌注模型,假手术组不予插线。手术前7天及术后24h内,羚蝎胶囊组灌喂羚蝎胶囊混悬液,其余两组分别灌喂0.9%的NaCl溶液。术后24h取材,检测脑组织超氧化物歧化酶（SOD）和丙二醛（MDA）的含量。结果与模型组相比,羚蝎胶囊组的SOD水平明显升高,MDA水平显著下降,两组差异有统计学意义（P〈0.05）。结论羚蝎胶囊可保护脑组织缺血再灌注后引发的自由基损伤,其作用可能与减轻缺血再灌注后脑组织的损害有关。     

原花青素对大鼠脑缺血再灌注损伤Caspase-3和Caspase-9活性的影响

目的 探讨原花青素(procyanidin,PC)对脑缺血再灌注损伤大鼠Caspase-3和Caspase-9活性的影响.方法 将大鼠随机分为假手术组、缺血再灌注组、PC低剂量治疗组和PC高剂量治疗组,线栓法建立局灶性脑缺血再灌注模型.采用四肽酶底物法检测脑缺血90 min再灌注24 h大鼠Caspase-3和Caspase-9活性,进行神经症状评分,2,3,5-三苯基氯化四氮唑(TTC)染色和HE染色观察脑梗塞体积及病理形态学变化.结果 脑缺血再灌注24 h,缺血再灌注组Caspase-3和Caspase-9活性增加,与假手术组比较,差异具有显著性(均P<0.05);与缺血再灌注组比较,PC高、低剂量治疗组均显著减少Caspase-3和Caspase-9活性,高、低剂量组之间差异亦具有显著性(P<0.05).PC高、低剂量治疗组神经功能缺失评分较缺血再灌注组降低(P<0.05).PC高、低剂量治疗组脑梗死体积较缺血再灌注组减小,高、低剂量组之间差异具有显著性(P<0.05).PC高、低剂量治疗组脑组织缺血损伤病理学改变明显轻于缺血再灌注组,PC高剂量治疗组缺血改变亦轻于低剂量治疗组.结论 PC对缺血再灌注脑损伤具有保护作用,其机制可能与减少Caspase-3和Caspase-9活性,抗凋亡有关.