17-β雌二醇对血管性痴呆大鼠认知功能和神经营养因子表达的影响

目的 研究17-β雌二醇对血管性痴呆(vascular dementia,VD)大鼠认知功能及脑组织神经生长因子(NGF)和脑源性神经营养因子(BDNF)表达的影响.方法 采用结扎双侧颈总动脉方法制备慢性前脑缺血动物模型,应用Y迷宫,免疫组化法和ELISA法检测腹腔注射17-β雌二醇60d后VD大鼠认知功能以及脑组织中NGF和BDNF含量变化.结果 与正常对照组对比,大鼠学习尝试次数,记忆测试10次的正确次数在造模60d后差异有显著性意义(P＜0.01),腹腔注射17-β雌二醇60d后,大鼠认知功显著改善;造模60d后的大鼠,其脑内NGF和BD-NF的含量较正常对照组显著增高,雌二醇组大鼠脑组织内NGF和BDNF的含量较模型组显著增高.结论腹腔注射17-β雌二醇可显著改善VD大鼠的认知功能,增加VD大鼠脑内NGF和BDNF含量.     

17-β雌二醇对血管性痴呆大鼠BDNF表达的影响

目的　研究 17-β雌二醇对血管性痴呆 (vasculardementia ,VD)大鼠脑组织脑源性神经营养因子 (BNDF)表达的影响。方法　采用结扎双侧颈总动脉方法制备慢性前脑缺血动物模型 ,应用Y迷宫 ,免疫组化及ELISA法等检测腹腔注射 17-β雌二醇60d后VD大鼠认知功能以及脑组织中BDNF含量变化。结果　与正常对照组对比 ,大鼠学习尝试次数 ,记忆测试 10次的正确次数在造模 60d后差异有显著性意义 (P <0 0 1) ,腹腔注射 17-β雌二醇 60d后 ,大鼠认知功能显著改善 ;造模 60d后的大鼠 ,其脑内BD NF免疫阳性细胞数较正常对照组显著增高 ,雌二醇组大鼠脑组织内BDNF免疫阳性细胞数较模型组显著增高。BDNF在三组大鼠脑内含量的测定结果与之一致。结论　腹腔注射 17-β雌二醇可显著改善VD大鼠的认知功能 ,增加VD大鼠脑内BDNF含量。     

酸性肽对AD大鼠学习记忆功能及NGF和NMDAR1表达的影响

目的 研究酸性肽对AD大鼠脑中NGF、NMDAR1表达的影响.方法 采用大鼠脑组织立体定位微量注射技术,建立AD动物摸型,用不同剂量的AP对AD大鼠进行治疗.通过测定与学习记忆有关的行为学指标及脑内与AD相关的NGF、AB水平的变化,并与正常组、模型组、生理盐水组结果 比较,对数据进行统计处理.结果 模型组与正常组比较,学习记忆成绩明显下降(P＜0.01);各治疗组与模型组比较,学习记忆成绩明显提高(P＜0.01);模型组与空白组比较,大鼠基底前脑中NGF水平显著降低,皮质中NMDAR1含量显著增加,各治疗组分别与模型组比较,大鼠基底前脑中NGF水平显著降低,皮质中NMDAR1含量显著增加(P＜0.01).结论 AP可能通过上调AD基底前脑中NGF的水平并降低NMDAR1水平来发挥对AD的治疗作用.     

盐酸美金刚对血管性痴呆大鼠海马CA1区BDNF及ERK表达的影响

目的 探讨盐酸美金刚对血管性痴呆大鼠海马神经元脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)及细胞外信号调节激酶(ERK)表达的影响.方法 健康雄性Wistar大鼠48只随机分为假手术组、模型组、盐酸美金刚组各16只,采用结扎双侧颈总动脉方法制备动物模型,用盐酸美金刚溶液灌胃,Y-型迷宫测试学习记忆能力,HE染色观察大鼠海马神经元的形态学变化,兔疫组化染色检测BDNF及ERK的表达变化.结果 盐酸美金刚组大鼠的学习记忆成绩优于模型组,但不及假手术组,差异均有统计学意义(P＜0.01);BDNF表达较模型组与假手术组均明显增高(P＜0.01) ; ERK表达较模型组明显增高,却低于假手术组,差异均有统计学意义(P＜0.01).结论 盐酸美金刚有可能通过增加VD大鼠脑内BDNF含量,保护海马神经元,增加ERK含量,改善学习记忆能力.     

银丹心脑通软胶囊对血管性痴呆模型大鼠行为学及脑组织自由基代谢的影响

目的 研究银丹心脑通(YDXNT)软胶囊对血管性痴呆(VD)模型大鼠学习记忆能力及超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量的影响. 方法 30只SD大鼠按照随机数字表法分成3组:假损伤组、VD模型组、YDXNT治疗组.后2组采用血管闭塞法复制VD模型,假损伤组除不结扎双侧颈总动脉外,其余处理与VD模型组、YDXNT治疗组相同.大鼠术后当天清醒后开始灌胃给药,YDXNT治疗组参照人的给药剂量,每只每次灌服lrnL液体(预先取YDXNT胶囊9粒去除胶囊溶解于360 mL生理盐水中配成液体备用),3次/d,连续注射4周.假损伤组与VD模型组均灌胃等体积生理盐水.Morris水迷宫检测大鼠学习记忆能力,放射免疫方法检测海马组织SOD活性与MDA含量. 结果 YDXNT治疗组大鼠找到平台的时间较VD模型组明显缩短,找到平台的游泳距离较VD模型组明显减少,差异均有统计学意义(P＜0.05).与VD模型组大鼠比较,YDXNT治疗组大鼠SOD活性明显升高,MDA含量明显降低,差异均有统计学意义(P＜0.05). 结论 YDXNT胶囊可增加脑组织氧自由基代谢能力,改善VD大鼠学习记忆能力.     

美满霉素改善血管性痴呆大鼠认知功能损伤并抑制氧化应激

目的 观察美满霉素(minocycline)对血管性痴呆大鼠学习记忆功能和脑组织内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)、诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)表达的影响,探讨美满霉素对血管性痴呆的脑保护作用的机制.方法 Wistar大鼠随机分为假手术组(S组)、痴呆模型组(M组)、美满霉素治疗组(MT组).RT-PCR和免疫组织化学法检测大鼠脑组织eNOS、iNOS的表达,行为学检测大鼠学习记忆功能的改变.结果 M组与S组行为学检查显示,M组大鼠有显著学习记忆障碍(P＜0.01),MT组与M组比较行为学检测结果显示,MT组大鼠学习记忆障碍有显著改善(P＜0.01).MT组iNOS表达较M组降低(P＜0.01),MT组eNOS表达较M组增高(P＜0.05);MT组eNOS、iNOS表达较S组增高(P＜0.01);M组eNOS、iNOS表达较S组显著增高(P＜0.01).结论 美满霉素能降低血管性痴呆大鼠脑组织iNOS表达,增强eNOS表达,抑制氧化应激反应,发挥脑保护作用.     

神经生长因子联合康复训练对脑梗死大鼠神经行为学及脑源性神经营养因子、Bax表达的影响

目的 研究神经生长因子(NGF)联合康复训练对脑梗死大鼠神经行为学及脑源性神经营养因子(BDNF)和促凋亡蛋白Bax表达的影响.方法 将72只SD大鼠随机分为对照组、NGF组、康复训练组及NGF联合康复训练治疗组(联合治疗组),每组又分为脑梗死后7d、14 d、21 d 3个亚组.采用线栓法制作脑梗死大鼠模型,NGF组制模后即予腹腔注射鼠NGF 20 μg/(kg·d);康复训练组制模后72 h给予平衡木、转棒、网屏训练;联合治疗组同时给予NGF和康复训练.各组分别于相应时间点进行神经行为学评分,采用免疫组化染色检测脑组织BDNF、Bax的表达,逆转录-PCR法检测BDNF mRNA、BaxmRNA的表达.结果 与对照组相比,NGF组、康复训练组及联合治疗组各时间点亚组的神经行为学评分均明显降低,脑组织BDNF、BDNFmRNA表达明显升高,Bax及Bax mRNA表达明显降低(均P＜0.05).与联合治疗组比较,NGF组、康复训练组各时间点亚组的神经行为学评分均明显升高,脑组织BDNF、BDNF mRNA水平明显降低,Bax、Bax mRNA表达水平明显增高(均P＜0.05).结论 NGF联合康复训练能上调BDNF、下调Bax的表达,而显著改善脑梗死大鼠的神经功能恢复.     

脑脉泰对慢性脑缺血大鼠认知功能的保护作用及其机制研究

目的研究脑脉泰影响脑组织神经生长因子(NGF)、胶质纤维酸性蛋白(GFAP)的表达,进而改善慢性脑缺血大鼠的认知功能。方法采用大鼠双侧颈总动脉永久结扎法(2-VO)制备慢性脑缺血模型。术后分别给予脑脉泰不同剂量灌胃治疗6 w。应用Morris水迷宫测定大鼠的学习记忆能力、HE染色观察海马CA1区神经元形态、免疫组化方法检测大鼠脑组织NGF及GFAP的表达。结果与假手术组相比,模型组大鼠的学习能力和记忆能力降低,脑组织中NGF表达减少(P<0.01),GFAP表达增多(P<0.01);脑脉泰给药能够改善大鼠的记忆和学习能力,增加脑组织中NGF表达(与模型组相比,低剂量组P<0.05,高剂量组P<0.01),降低GFAP表达(与模型组相比,低、高剂量均为P<0.01)。结论脑脉泰可能通过提高脑组织NGF和降低GFAP表达来改善慢性脑缺血大鼠的认知功能。     

银丹心脑通软胶囊对血管性痴呆大鼠学习记忆能力及皮层反应性氮中介物含量的影响

目的 探讨银丹心脑通软胶囊对血管性痴呆(VD)大鼠学习记忆能力及大脑皮层反应性氮中介物含量的影响. 方法 将SD大鼠按随机数字表法分为假手术组、VD组、银丹心脑通软胶囊治疗组,后两组采用永久性结扎双侧颈总动脉方法制备VD模型,银丹心脑通软胶囊治疗组于手术后即刻给予银丹心脑通软胶囊60 mg/(kg·d)灌胃,连续给药4周.4周后采用Morris水迷宫试验观察各组大鼠学习记忆能力的改变,采用比色法检测大鼠大脑皮层一氧化氮(NO)、诱导型一氧化氮合酶(iNOS)含量的变化. 结果 VD组与银丹心脑通软胶囊治疗组、假手术组比较,逃避潜伏期明显延长,原平台所在象限的搜索时间明显缩短,差异有统计学意义(P＜0.05).银丹心脑通软胶囊治疗组较VD组逃避潜伏期明显缩短、原平台所在象限的搜索时间明显延长,差异有统计学意义(P＜0.05).银丹心脑通软胶囊治疗组与VD组相比,大脑皮层NO和iNOS含量明显下降,差异有统计学意义(P＜0.05). 结论 银丹心脑通软胶囊能降低VD大鼠皮层NO、iNOS含量,对学习记忆能力有明显的提高作用.     

17-β雌二醇对血管性痴呆大鼠认知功能及脑内GDNF表达的影响

目的 研究17-β雌二醇对血管性痴呆(VD)大鼠脑组织胶源性神经营养因子(GNDF)表达的影响.方法 结扎双侧颈总动脉制备慢性前脑缺血动物模型,应用Y迷宫,免疫组化检测腹腔注射17-β雌二醇60d后血管性痴呆大鼠认知功能以及脑组织中GDNF表达.结果 与正常对照组对比,大鼠学习尝试次数,记忆测试10次的正确次数在造模60d后差异有统计学意义(P＜0.01),腹腔注射17-β雌二醇60d后,大鼠认知功显著改善;造模60d后的大鼠,其脑内GDNF免疫阳性细胞数较正常对照组显著增高,雌二醇组大鼠脑组织内GDNF免疫阳性细胞数较模型组显著增高.结论 腹腔注射17-β雌二醇可显著改善VD大鼠的认知功能,增加VD大鼠脑内GDNF表达.     

支气管哮喘大鼠肺内神经营养因子对气道高反应性影响的研究

目的 探讨支气管哮喘大鼠肺内神经营养因子水平的变化,及其与气道神经可塑性改变和气道高反应性间的关系. 方法 雄性SD大鼠40只按随机数字表法分为对照组、哮喘组、神经生长因子(NGF)+脑源性神经营养因子(BDNF)干预组和anti-NGF+anti-BDNF干预组(每组各10只),后三组通过鸡卵蛋白致敏激发建立哮喘模型并给予相应的干预.造模后第8周进行气道阻力测定,并留取左肺行HE染色及免疫组化染色检测肺组织中神经营养因子如NGF、BDNF的表达水平,RT-PCR法检测气道突触囊泡素(SYN)mRNA和神经丝(NF)mRNA的表达水平. 结果 哮喘组及NGF+BDNF干预组大鼠肺组织内可见大量炎症细胞浸润.哮喘组大鼠肺组织中NGF及BDNF的表达水平均明显高于对照组及anti-NGF+anti-BDNF干预组,差异有统计学意义(P＜0.05),而NGF+BDNF干预组肺组织中NGF及BDNF的表达水平明显高于哮喘组,差异亦有统计学意义 (P＜0.05).哮喘组及NGF+BDNF干预组较对照组的气道反应性增高,气道感觉神经元SYN mRNA及NF mRNA的表达水平也明显增高,差异均有统计学意义(P＜0.05).哮喘组大鼠肺组织中NGF及BDNF浓度与气道SYN表达呈正相关关系(r=0.889,P＜0.05;r=0.985,P＜0.05),与NF表达呈正相关关系(r=0.956,P＜0.05;r=0.927,P＜0.05),与气道反应性也呈正相关关系(r=0.938,P＜0.05;r=0.906,P＜0.05). 结论 NGF及BDNF可能参与了支气管哮喘大鼠气道神经可塑性改变的调节过程,从而导致气道高反应性的发生.     

静脉注射人脐血间充质干细胞对脑损伤神经生长因子的影响

目的 观察TBI后静脉注射人脐血间充质干细胞(CB-MSCs)对NGF、BDNF表达的影响,探讨其脑保护的作用机制.方法 清洁级健康雄性SD大鼠90只采用完全随机数字表法分为假手术组、损伤组和治疗组,每组30只.损伤组和治疗组采用改进的Feeney自由落体法制作大鼠TBI模型,假手术组只开骨窗,不撞击硬脑膜.治疗组尾静脉注入3×106个Brdu标记的CB-MSCs,损伤组及假手术组注入等体积的PBS液.在移植后3、7、14、21、28 d,采用HE染色、免疫组化染色、原位杂交法对TBI大鼠脑组织形态学变化、Brdu标记情况、NGF和BDNF表达情况进行检测.结果 假手术组仅有极少量的NGF、BDNF阳性表达细胞.损伤组表达明显增加,以损伤周边区最为明显,注射后14d达到高峰(NGFA值为8.35±1.07,BDNFA值为9.01±1.74),之后逐渐下降,但仍高于假手术组,差异有统计学意义(P＜0.05).治疗组表达趋势与损伤组相同,14d达高峰后,21 d、28 d阳性表达明显下降;各时间点均高于损伤组与假手术组,差异有统计学意义(P＜0.05).结论 在TBI中,静脉注射CB-MSCs可以增加损伤局部NGF、BDNF的分泌,改善局部微环境,促进神经元的修复.     

Functional recovery and microenvironmental alterations in a rat model of spinal cord injury following human umbilical cord blood-derived mesenchymal stem cells transplantation

BACKGROUND: Transplantation of human umbilical cord blood-derived mesenchymal stem cells (MSCs) has been shown to benefit spinal cord injury (SCI) repair. However, mechanisms of microenvironmental regulation during differentiation of transplanted MSCs remain poorly understood. OBJECTIVE: To observe changes in nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and interleukin-8 (IL-8) expression following transplantation of human umbilical cord-derived MSCs, and to explore the association between microenvironment and neural functional recovery following MSCs transplantation.DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the Department of Orthopedics, First Affiliated Hospital of Soochow University from April 2005 to March 2007. MATERIALS: Human cord blood samples were provided by the Department of Gynecology and Obstetrics, First Affiliated Hospital of Soochow University. Written informed consent was obtained. METHODS: A total of 62 Wister rats were randomly assigned to control (n = 18), model (n = 22, SCI + PBS), and transplantation (n = 22, SCI + MSCs) groups. The rat SCI model was established using the weight compression method. MSCs were isolated from human umbilical cord blood and cultured in vitro for several passages. 5-bromodeoxyuridine (BrdU)-labeled MSCs (24 hours before injection) were intravascularly transplanted. MAIN OUTCOME MEASURES: The rats were evaluated using the Basso, Beattie and Bresnahan (BBB) locomotor score and inclined plane tests. Transplanted cells were analyzed following immunohistochemistry. Enzyme-linked immunosorbant assay was performed to determine NGF, BDNF, and IL-8 levels prior to and after cell transplantation.RESULTS: A large number of BrdU-positive MSCs were observed in the SCI region of the transplantation group, and MSCs were evenly distributed in injured spinal cord tissue 1 week after transplantation. BBB score and inclined plane test results revealed significant functional improvement in the transplantation group compared to the model group (P< 0.05), which was maintained for 2-3 weeks. Compared to the model group, NGF and BDNF levels were significantly increased in the injured region following MSCs transplantation at 3 weeks (P < 0.05), but IL-8 levels remained unchanged (P > 0.05).CONCLUSION: MSCs transplantation increased NGF and BDNF expression in injured spinal cord tissue. MSCs could promote neurological function recovery in SCI rats by upregulating NGF expression and improving regional microenvironments.     

驽药针刺对大鼠脊髓损伤后运动功能及BDNF表达的影响

目的研究驽药针刺在大鼠脊髓损伤后运动功能变化以及BDNF表达的变化。方法采用脊髓半横断损伤模型。100只SD大鼠随机分为对照组、假手术组、脊髓损伤组、单纯针刺组、驽药针刺组,每组分为3天、7天、14天、21天共4个亚组,每组5只。BBB法评定大鼠后肢运动功能变化,免疫组化法检测大鼠脊髓中BDNF的表达变化。结果 BBB评分显示驽药针刺组的各时间点评分均高于脊髓损伤组(P0.05),驽药针刺组7、14、21d的BDNF表达均高于脊髓损伤组(P0.05),且与BBB评分呈正相关(r=0.717,P0.05)。结论驽药针刺可明显改善脊髓损伤大鼠的运动功能,并可明显促进大鼠脊髓损伤后BDNF的表达。     

大鼠局灶性脑缺血后神经营养因子表达的自然变化

目的 观察大鼠局灶性脑缺血后大鼠神经行为、梗死体积、组织形态及缺血半暗带神经生长因子(NGF)、脑源性神经营养因子(BDNF)的表达水平变化。方法 将健康雄性SD大鼠24只随机分为2组,Ⅰ组(假手术组); Ⅱ组(脑缺血组)。用线栓法建立动物模型,不给予再灌注,各组在术后48h断头取脑,处死前行神经功能评分,用氯化三苯基四氮唑(TTC)染色计算脑梗死体积,用HE染色观察组织学形态,用免疫组织化学染色观察NGF、BDNF的表达水平。结果 Ⅰ组在神经功能评分、梗死体积、组织形态及大脑皮层相应部位NGF、BDNF阳性细胞数均正常。与Ⅰ组比较,Ⅱ组的神经功能评分和梗死体积均严重受损; 光镜下Ⅱ组缺血性病理改变较重,与Ⅰ组比较,Ⅱ组缺血半暗带NGF、BDNF阳性神经元数增加(P<0.05)。结论 脑缺血本身可上调缺血半暗带NGF、BDNF的表达水平。     

慢性脑低灌注对大鼠皮层核因子E2相关因子2表达的影响

目的 研究慢性脑低灌注大鼠皮层核因子E2相关因子2(Nrf2)的表达.方法 用随机数字表法将大鼠分为双血管结扎术(2VO)-3周组、2VO-8周组和假手术组,2VO术式制备慢性脑低灌注大鼠模型并在相应时间点取材,采用免疫组化染色、实时定量PCR方法检测大鼠皮层Nrf2的表达,用硫代巴比妥酸法测定丙二醛(MDA)含量.结果 免疫组化染色结果显示,与假手术组(38.01%±4.51%)相比,2VO-3周组(50.18%±14.22%)、2VO-8周组(23.15%±7.42%)大鼠皮层Nrf2阳性细胞比例差异均无统计学意义(P＞0.05);与2VO-3周组相比,2VO-8周组大鼠皮层Nrf2阳性细胞比例明显降低,比较差异有统计学意义(P＜0.05).实时定量PCR结果提示,2VO-8周组大鼠皮层Nrf2 mRNA的表达(相对扩增倍数)较2VO-3周组降低,但差异无统计学意义(P＞0.05).生化检测发现,与假手术组[(3.894±0.512)nmol/mg]相比,2VO-8周组大鼠皮层MDA含量[(6.855±1.351)nmol/mg]明显升高,比较差异有统计学意义(P＜0.05).结论 慢性脑低灌注大鼠皮层MDA含量随时间延长而不断增加,除3周时蛋白表达上调外,Nrf2蛋白与mRNA水平均有不同程度减低,提示慢性脑低灌注状态时氧化性损伤持续加重,这可能与内源性抗氧化系统受到抑制有关.

Abstract：

Objective To examine the effect of chronic cerebral hypoperfusion (CCH) on the expression of nuclear factor E2-related factor 2 (Nrf2) in rat cortex. Methods Rats were randomly divided into 2 operated groups and a sham-operated group; rat models of chronic cerebral hypoperfusion in the 2 operated groups were established by occlusion of bilateral common carotid arteries (2VO) for 3 and 8 weeks, respectively. The RNA and protein contents of Nrf2 in the cortex were detected by immunohistochemistry and real-time quantitative PCR, respectively, and the content of malonaldehyde (MDA) was measured by thiobarbituric acid-reactive substance assay. Results A significantly lower percentage of Nrf2-positive cells in the cortex of 2VO-8w group (23.15%±7.42%) was noted as compared with that in the 2VO-3w group (50.18%±14.22%) (P＜0.05); no significant differences on the percentage of Nrf2-positive cells were noted between the sham-operated group (38.01%±4.51%) and the 2 operated groups (P＞0.05). Though the RNA content of Nrf2 in the cortex of 2VO-8w group (0.993 ±0.492)decreased as compared with that in the 2VO-3w group (1.536±0.493)(P＞0.05), no statistical difference was noted between the sham-operated group (1.690± 1.195) and both the 2VO-3w group and the 2VO-8w group (P＞0.05). And the content of MDA in the 2VO-8w group ([6.855±1.351] nmol/mg) was significantly increased as compared with that in the sham-operated group ([3.894±0.512] nmol/mg) (P＜0.05). Conclusion The content of MDA keeps increasing. Additionally, except the protein expression up-regulates 3 weeks after occlusion, the RNA and protein expressions of Nrf2 in rat cortex are down-regulated with the process of CCH, suggesting that oxidative damage become much severe with theprocess of CCH, which may be partly attributed to the dysfunction of endogenous antioxidative mechanisms.     

Effects of brain-derived neurotrophic factor and nerve growth factor on remaining neurons in the lesioned nucleus basalis magnocellularis

Rats received a unilateral lesion of the nucleus basalis magnocellularis (NBM) by infusion of ibotenic acid. Starting 2 weeks after the lesion, the animals were treated with nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF) by intraparenchymal infusion of 3 μg per day for 4 weeks. Lesioned control animals received a similar amount of cytochromec. The activity of cholone acethyltransferase (ChAT) in the frontal neocortex was signigicantly reduced by the lesion (−39%). However, the intraparenchymal treatment with NGF or BDNF did not affect cortical ChAT activity. The number of p75 NGF receptor-immunoreactive neurons in the NBM was significantly decreased (−49%) by the lesion and was not affected by NGF or BDNF. The size of the remaining neurons was significantly increased by NGF (+32%), but not by BDNF (+12%). Similarly, in situ hybridization showed enhanced expression of the p75 NGF receptor following treatment with NGF, but not with BDNF. These results suggest that although BDNF occurs in the target area of cholinergic NBM neurons, its effects on these neurons are less pronounced than those of NGF.     

电针对MCAO大鼠皮层神经营养因子表达的影响

目的　应用免疫组织化学法观察电针对缺血皮层神经元脑源性神经营养因子 (BDNF)和神经生长因子 (NGF)表达的影响。方法　实验分缺血组和缺血 电针组 ,大脑中动脉线栓 (MCAO)造成局灶性缺血 75 m in,缺血 电针组在缺血后立即给予电针 1h。在缺血再灌不同时间分别处死 ,然后进行免疫组织化学染色。结果　 BD-NF和 NGF主要在缺血灶周围的皮层表达。在再灌后 8h内缺血 电针组 BDNF和 NGF免疫阳性细胞的表达高于缺血组 (P<0 .0 1)。结论　电针能够提高 NGF和 BDNF在缺血灶周围皮层的表达 ,这种高表达可能对脑缺血具有保护作用。     

不同刺激参数rTMS对慢性不可预见应激大鼠行为的作用及大脑BDNF水平的影响

目的 观察不同刺激参数重复经颅磁刺激（rTMS）对慢性不可预见应激（CUS）模型大鼠行为学的作用,并观察其对大鼠脑源性神经营养因子（BDNF）水平的影响.方法 64只SD大鼠随机分为对照组（8只）、模型组（8只）和干预组（共6个亚组,每组8只）.对照组正常饲养21d后连续7d给予rTMS假刺激;模型组在造模后连续7d给予rTMS假刺激;干预组在造模后每天给予不同频率和强度的rTMS刺激,连续7d.实验期间观察大鼠体质量的变化,并采用运动箱和强迫游泳实验评估大鼠抑郁样行为,最后以酶联免疫吸附法测定大脑BDNF的水平.结果 （1）造模结束后,对照组大鼠的体质量、强迫游泳静止时间与其他两组相比均存在显著性差异（P＜0.01,P＜0.05）,而模型组和干预组大鼠比较没有上述差异（P＞ 0.05）.各组大鼠水平运动距离没有显著性差异（P＞0.05）.（2）rTMS干预后,①模型组大鼠的体质量显著低于对照组及干预组（5 Hz,0.84/1.26 T和10 Hz,0.84/1.26 T） （P ＜0.05）.②各组大鼠水平运动距离之间没有显著性差异;模型组强迫游泳静止时间百分比明显高于对照组及干预组（P＜0.05）.③模型组BDNF的水平低于对照组,而一定刺激条件的rTMS可以改善这一现象.④双因素方差分析显示,刺激频率可能是改善大鼠抑郁行为和调节BDNF的关键因素,而且5 Hz的抗抑郁效应更为显著.结论 不同刺激参数的rTMS对CUS动物抑郁行为的改善作用存在差异,大脑BDNF水平的变化可能参与了这一改善过程.     

Study on molecular mechanism for improving neural regeneration after repair of sciatic nerve defect in rat by acellular nerve allograft

Objective: Discuss the molecular mechanism for improving neural regeneration after repair of sciatic nerve defect in rat by acellular nerve allograft (ANA). Methods: Randomly divide 36 Wistar rats into six groups as normal control group, autografting group, and bridging groups of 2, 4, 8, 12 weeks, six rats for each group. Observe the expression of brain‐derived neurotrophic factor (BDNF) in L₄ spinal cord and anterior tibial muscle at the injury site, calcitonin gene‐related peptide (CGRP) protein as well as mRNA, respectively. 12w after operation, histopathological observation was performed. Results: 2w after ANA bridging the sciatic nerve defect in rats, it was observed that the expression level of BDNF in spinal cord at the injury site and CGRP protein increased, reaching the peak level at 4w, lasting till 8w, then decreased but still significantly higher than that in normal control group at 12w, and was not significantly different compared with that in autografting group. However, the expression level of BDNF in anterior tibial muscle decreased gradually within the initial 4w, then increased progressively, reaching normal level at 12w, and was not significantly different compared with that in autografting group. The expression of BDNF mRNA and CGRPmRNA was essentially the same. 12w after operation, there was nerve regeneration in bridging group of 12w and autografting group. Conclusions: ANA possessed fine histocompatibility, and might substitute autograft to repair long‐segment defect of sciatic nerve in rats. This action might be related to upregulation of protein and mRNA expression for BDNF and CGRP in spinal cord. Synapse, 2012. © 2011 Wiley Periodicals, Inc.