叶酸对脑梗塞大鼠神经细胞凋亡及Notch1 mRNA表达的影响

目的研究叶酸(FA)对脑梗塞大鼠缺血侧脑组织内神经细胞凋亡及Notch1 mRNA表达的影响。方法雄性SD大鼠48只按体重随机分为4组:假手术组(SO)、大脑中动脉梗塞组(MCAO)、MCAO+叶酸低剂量组(MCAO+LFA)、MCAO+叶酸高剂量组(MCAO+HFA)。除SO组外,其他三组均采用线拴法制作大鼠大脑中动脉栓塞,各组于栓塞处理后第14天处死。补充叶酸前、补充28天后及栓塞处理后第14天,采用化学发光免疫法测定各组大鼠血清叶酸含量;建立MCAO后第14天,应用TUNEL法测定缺血侧脑组织内神经细胞的凋亡,荧光原位杂交法检测神经细胞内Notch1 mRNA的表达。结果补充叶酸后,与MCAO组相比,MCAO+LFA、MCAO+HFA组神经细胞凋亡率明显降低(P<0.01),血清叶酸浓度及Notch1 mRNA的荧光强度值均明显升高(P<0.01)。结论叶酸降低脑梗塞大鼠神经细胞凋亡率可能与其促进Notch1 mRNA的表达有关。     

Upregulation of Vitamin C Transporter Functional Expression in 5xFAD Mouse Intestine

The process of obtaining ascorbic acid (AA) via intestinal absorption and blood circulation is carrier-mediated utilizing the AA transporters SVCT1 and SVCT2, which are expressed in the intestine and brain (SVCT2 in abundance). AA concentration is decreased in Alzheimer’s disease (AD), but information regarding the status of intestinal AA uptake in the AD is still lacking. We aimed here to understand how AA homeostasis is modulated in a transgenic mouse model (5xFAD) of AD. AA levels in serum from 5xFAD mice were markedly lower than controls. Expression of oxidative stress response genes (glutathione peroxidase 1 (GPX1) and superoxide dismutase 1 (SOD1)) were significantly increased in AD mice jejunum, and this increase was mitigated by AA supplementation. Uptake of AA in the jejunum was upregulated. This increased AA transport was caused by a marked increase in SVCT1 and SVCT2 protein, mRNA, and heterogeneous nuclear RNA (hnRNA) expression. A significant increase in the expression of HNF1α and specific protein 1 (Sp1), which drive SLC23A1 and SLC23A2 promoter activity, respectively, was observed. Expression of hSVCT interacting proteins GRHPR and CLSTN3 were also increased. SVCT2 protein and mRNA expression in the hippocampus of 5xFAD mice was not altered. Together, these investigations reveal adaptive up-regulation of intestinal AA uptake in the 5xFAD mouse model.     

Dietary L-arginine supplementation enhances endothelial nitric oxide synthesis in streptozotocin-induced diabetic rats

This study tested the hypothesis that dietary arginine supplementation increases endothelial tetrahydrobiopterin (BH(4)) availability for nitric oxide (NO) synthesis in diabetic rats. Streptozotocin-induced diabetic rats either were given unrestricted access to a casein-based diet (Expt. 1) or were pair-fed the diet on the basis of the food intake per kg of body weight of nondiabetic rats (Expt. 2). Beginning 1 d after vehicle or streptozotocin injection, arginine-HCl (1.51%) or alanine (isonitrogenous control, 2.55%) was added daily to the drinking water for nondiabetic rats, whereas concentrations were adjusted (0.43% arginine-HCl and 0.73% alanine) in the drinking water for diabetic rats (which consumed more water) to ensure isonitrogenous provision. At 2 wk after the initiation of arginine supplementation, coronary endothelial cells and plasma were obtained for the measurement of NO synthesis and metabolites. In both experiments, plasma and endothelial concentrations of N(G)-monomethylarginine, asymmetric dimethylarginine, and symmetric dimethylarginine increased, but those of arginine as well as endothelial BH(4) availability and NO synthesis decreased in diabetic rats, compared with nondiabetic rats. In both diabetic and nondiabetic rats, arginine supplementation increased plasma concentrations of arginine and insulin, endothelial concentrations of arginine and BH(4), and endothelial NO synthesis, but did not affect plasma and endothelial concentrations of methylarginines or plasma concentrations of homocysteine. Dietary arginine supplementation or provision of a BH(4) precursor normalized endothelial NO synthesis in diabetic rats. Arginine supplementation did not affect plasma glucose levels in nondiabetic rats, but reduced body weight loss and plasma glucose levels in diabetic rats. Thus, dietary L-arginine supplementation stimulates endothelial NO synthesis by increasing BH(4) provision, which is beneficial for vascular function and glucose homeostasis in diabetic subjects.     

局灶性脑缺血大鼠脑中血小板内皮细胞黏附分子-1、Bel-2和Bax表达的动态改变

目的观察大鼠局灶性脑缺血后脑组织中血小板内皮细胞黏附分子-1（PECAM-1、CD31）、Bcl-2、Bax表达的动态改变。方法采用线栓法制作大鼠大脑中动脉局灶性脑缺血模型，脑组织切片免疫组化染色检测不同时间点PECAM．1、Bcl-2、Bax在脑组织中的表达变化。结果大鼠大脑中动脉闭塞后脑组织PECAM-1、Bcl-2、Bax的表达明显增高（均P〈0．001）。Bcl-2在闭塞后12h达到高峰，Bax在24h达高峰，PECAM-148h达高峰；至72h，三者仍明显高于对照组（P〈0．001）。结论脑组织表达的PECAM-1、Bcl-2、Bax分别参与了脑缺血不同时期的病理生理作用。     

Neuroprotective Effect of 1,3-dipalmitoyl-2-oleoylglycerol Derived from Rice Bran Oil against Cerebral Ischemia-Reperfusion Injury in Rats

1,3-Dipalmitoyl-2-oleoylglycerol (POP) is a triacylglyceride found in oils from various natural sources, including palm kernels, sunflower seeds, and rice bran. In the current study, the neuroprotective effects and the specific mechanism of POP derived from rice bran oil were investigated for the first time using the middle cerebral artery occlusion/reperfusion (MCAO/R) model in rats. Orally administered POP at 1, 3, or 5 mg/kg (three times: 0.5 h before MCAO, after 1 h of MCAO, and after 1 h of reperfusion) markedly reduced the MCAO/R-induced infarct/edema volume and neurobehavioral deficits. Glutathione depletion and the oxidative degradation of lipids in the rat brain induced by MCAO/R were prevented by POP administration. The upregulation of phosphorylated p38 MAPKs, inflammatory factors (inducible nitric oxide synthase (i-NOS) and cyclooxygenase-2 (COX-2)), and pro-apoptotic proteins (B-cell lymphoma-2 (Bcl-2) associated X protein (Bax) and cleaved caspase-3) and the downregulation of the anti-apoptotic protein (Bcl-2) in the ischemic brain were significantly inhibited by POP administration. In addition, downregulation of phosphatidylinositol 3′-kinase (PI3K), phosphorylated protein kinase B (Akt), and phosphorylated cyclic (adenosine monophosphate) AMP responsive element-binding protein (CREB) expression in the ischemic brain was inhibited by POP administration. These results suggest that POP might exert neuroprotective effects by inhibition of p38 MAPK and activation of PI3K/Akt/CREB pathway, which is associated with anti-oxidant, anti-apoptotic, and anti-inflammatory action. From the above results, the present study provides evidence that POP might be effectively applied for the management of cerebral ischemia-related diseases.     

外源性血管内皮生长因子基因在新生鼠缺氧缺血性脑损伤模型中的表达

目的:研究外源性血管内皮生长因子(VEGF)在新生鼠缺氧缺血脑损伤(Hypoxic-ischemic brain damageHIBD)模型中的表达情况。方法:构建了负载有鼠VEGF120 cDNA的真核表达质粒pCDNA3.1,建立新生鼠缺氧缺血脑损伤模型,将质粒注射至新生鼠缺氧缺血脑损伤局部,探讨外源性VEGF在新生鼠脑内的表达情况。应用VEGF免疫组织化学方法检测转移pCDNA3.1/rVEGF120真核表达质粒后大鼠脑中VEGF的表达情况。结果:与转移空载质粒的对照组相比,脑内注射外源性VEGF基因,在大脑皮质及海马的神经细胞、神经胶质细胞及血管内皮细胞胞浆中高度表达。结论:在HIBD模型中,脑内注射的外源性VEGF基因在大脑皮质及海马处神经细胞、胶质细胞、血管内皮细胞胞浆中高度表达。     

S-allyl cysteine mitigates oxidative damage and improves neurologic deficit in a rat model of focal cerebral ischemia

Oxidative stress and inflammatory damage play an important role in cerebral ischemic pathogenesis and may represent a target for treatment. The present study examined the hypothesis that S-allyl cysteine (SAC), organosulfur compounds found in garlic extract, would reduce oxidative stress–associated brain injury after middle cerebral artery occlusion (MCAO). To test this hypothesis, male Wistar rats were subjected to MCAO for 2 hours and 22-hour reperfusion. S-allyl cysteine was administered (100 mg/kg, b.wt.) intraperitoneally 30 minutes before the onset of ischemia and after the ischemia at the interval of 0, 6, and 12 hours. After 24 hours of reperfusion, rats were tested for neurobehavioral activities and were killed for the infarct volume, estimation of lipid peroxidation, glutathione content, and activity of antioxidant enzymes (glutathione peroxidase, glutathione reductase, catalase, and superoxide dismutase). S-allyl cysteine treatment significantly reduced ischemic lesion volume, improved neurologic deficits, combated oxidative loads, and suppressed neuronal loss. Behavioral and biochemical alterations observed after MCAO were further associated with an increase in glial fibrillary acidic protein and inducible nitric oxide expression and were markedly inhibited by the treatment with SAC. The results suggest that SAC exhibits exuberant neuroprotective potential in rat ischemia/reperfusion model. Thus, this finding of SAC-induced adaptation to ischemic stress and inflammation could suggest a novel avenue for clinical intervention during ischemia and reperfusion.     

丹参酮ⅡA对脑缺血再灌注损伤大鼠P-选择素和细胞间黏附分子-1表达的影响

目的探讨丹参酮ⅡA（TanⅡA）对脑缺血再灌注损伤大鼠P-选择素和细胞间黏附分子-1（ICAM-1）表达的影响。方法将大鼠随机分为假手术组、缺血再灌注组、TanⅡA低剂量治疗组和TanⅡA高剂量治疗组，线栓法建立局灶性脑缺血再灌注模型。TanⅡA治疗组于术前连续灌胃给药3d，1次／d。用免疫组化法观察缺血90min再灌注24h大鼠额顶部皮质P-选择素和ICAM-1表达，进行2，3，5-三苯基氯化四氮唑（TTC）染色和HE染色观察脑梗死体积及病理形态学变化。结果脑缺血再灌注24h，缺血再灌注组P-选择素和ICAM-1表达均明显增加，与假手术组比较，差异具有统计学意义（均P〈0．01）；与缺血再灌注组比较，TanⅡA低、高剂量治疗组均显著减少P-选择素和ICAM-1表达（均P〈0．01），低、高剂量组之间差异亦具有统计学意义（P〈0．01）；TanⅡA低、高剂量治疗组脑梗死体积较缺血再灌注组减小，低、高剂量组之间差异亦具有统计学意义（P〈0．01）；TanⅡA低、高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，TanⅡA高剂量治疗组缺血改变亦轻于低剂量治疗组。结论TanⅡA对缺血再灌注脑损伤具有保护作用，其机制可能与减轻脑缺血再灌注损伤阶段P-选择素和ICAM-1所介导的炎症反应有关，高剂量TanⅡA（30mg／kg）的保护效果更显著。     

电离辐射对大鼠脑皮质牛磺酸、谷氨酸及其谷氨酸阳性神经元的影响

目的 探讨电离辐射对大鼠脑皮质内谷氨酸(glutamate,Glu)、牛磺酸(taurine,Tau)水平和谷氨酸阳性神经元的影响。方法 雄性SD大鼠45只随机分为3组,头部分别给予0、10、20 Gy ⁶⁰Coγ射线照射。照射后12h测定脑皮质谷氨酸(Glu)、牛磺酸的含量以及神经细胞内游离Ca²⁺浓度([Ca²⁺]i),同时观察大鼠脑皮质Glu阳性神经元以及神经细胞凋亡情况。结果 随着照射剂量的增加,脑皮质内Glu含量升高,Tau含量减少,Glu/Tau比值逐渐上升,细胞内游离Ca²⁺浓度([Ca²⁺]i)升高,Glu阳性神经元数量增加,细胞凋亡数量上升,并与电离辐射呈一定的量效关系。结论 上述结果提示Glu产生的神经毒作用参与了电离辐射对中枢神经系统的损伤过程。     

VEGF对缺血脑组织表达Fas/Fasl的影响

目的探讨VEGF治疗脑梗死的机制.方法用线拴法制成Wistar大鼠大脑中动脉永久性闭塞模型,将VEGF165真核表达质粒pUCCAGGS/hVEGF165经颅骨注入到缺血区.术后7d断头取脑,用逆转录PCR(RT-PCR)检测VEGF mRNA的表达强度,用免疫组织化学方法检测Fas、Fasl和VEGF的表达水平.结果与对照组相比,治疗组VEGFmRNA的表达增强,VEGF表达增高(P＜0.01),Fas、Fasl表达减弱(P＜0.01).结论VEGF165基因可以转化到缺血脑组织中并表达VEGF mRNA和VEGF,后者可能通过抑制Fas和Fasl的表达而保护神经细胞.     

Folic acid enhances Notch signaling, hippocampal neurogenesis, and cognitive function in a rat model of cerebral ischemia

Increasing neurogenesis may restore cognitive functions that are impaired in ischemia stroke. Folic acid has been reported to play an important role in neuronal development and reduce the risk of ischemic stroke in primary prevention. Folic acid supplementation stimulates Notch signaling and cell proliferation in neural progenitor cells cultured from neonatal brain. The present study determined whether folic acid supplementation stimulates Notch signaling and neurogenesis and improves cognitive function after ischemic stroke in adult brain. Rats were randomly assigned to four groups: sham operation plus vehicle (Sham), middle cerebral artery occlusion plus vehicle (MCAO), MCAO plus low-dose folic acid (4 mg/(kg day)), and MCAO plus high folic acid (12 mg/(kg day)). The vehicle and folic acid were administered by oral gavage for 28 days prior to sham or MCAO operation and up to 14 days after surgery. Newborn hippocampal neurons were detected at 3, 7, and 14 days post-MCAO. Cognitive function (learning and memory in Y-maze tests) and the protein expression levels of components of the Notch signaling system (Notch1, Hes1, and Hes5) were measured at 7 days post-MCAO. The results showed that MCAO impaired Y-maze performance and stimulated Notch signaling and hippocampal neurogenesis in brain. Folic acid prevented the impairment of Y-maze performance. The nutrient also increased further the expression of Notch1, Hes1, and Hes5 and the number of the newborn hippocampal neurons. Folic acid enhances the stimulation by ischemia of Notch signaling and hippocampal neurogenesis in adult brain and lessens the impairment of cognitive function that occurs after experimental stroke.     

叶酸、维生素B_6、B_(12)对局灶性脑缺血大鼠血浆同型半胱氨酸水平和抗氧化作用的研究

目的:研究叶酸(FA)、维生素B6(VB6)和维生素B12(VB12)对局灶性脑缺血大鼠血浆同型半胱氨酸(homocysteine,Hcy)水平和抗氧化作用。方法:SD大鼠随机分为假手术组(Sham)、大脑中动脉闭塞模型组(MCAO)、MCAO+FA组和MCAO+FA+VB6+VB12组(MCAO+CV)。后三组均经手术造成MCAO模型,维生素补充前、补充28d后和手术后24h分别检测大鼠血浆Hcy浓度及血清超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和丙二醛(MDA)含量,缺血后检测脑组织抗氧化指标。结果:补充FA、VB6和VB12后及缺血后,MCAO+FA组和MCAO+CV组血浆Hcy均低于Sham组和MCAO组,且MCAO+CV组低于MCAO+FA组;MCAO+FA组和MCAO+CV组血清或脑组织SOD和GSH-Px活性均高于MCAO组,MDA含量低于MCAO组。结论:补充FA、VB6和VB12能降低血浆Hcy浓度,提高机体抗氧化能力,减轻脑缺血造成的氧化应激损伤。     

叶酸对局灶性脑缺血大鼠神经细胞凋亡的影响

目的观察叶酸(folic acid,FA)对局灶性脑缺血大鼠神经细胞凋亡的影响并探讨其作用机制。方法将32只成年雄性SD(Sprague-Dawley)大鼠随机分为假手术(SO)、大脑中动脉栓塞模型(MCAO)、缺血+叶酸低剂量(MCAO+FA-L)和缺血+叶酸高剂量(MCAO+FA-H)4组。除假手术组外,其他三组采用线栓法制作大鼠大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型,各组于造模后D7处死。叶酸补充前、补充28d后(造模前)和造模后D7分别检测血清中丙二醛(MDA)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性;采用TUNEL法检测脑组织细胞凋亡率;Western blotting方法检测磷酸化细胞外信号调节激酶(extracellular signaling-related kinase,ERK1/2)蛋白表达水平。结果与缺血模型组比,低、高剂量叶酸均可明显减少脑组织中凋亡细胞率(P<0.01),降低血清中MDA含量(P<0.01),提高SOD、GSH-Px活性水平(P<0.01),并增加磷酸化ERK1/2蛋白的表达。结论叶酸能降低神经细胞凋亡率,其作用机制可能与增强自由基清除酶活性,抑制脂质过氧化反应,或上调磷酸化ERK1/2蛋白有关。     

番茄红素对大鼠脑缺血再灌注损伤的影响

目的观察番茄红素(LP)对大鼠局灶性脑缺血再灌注损伤(I/R)及机体氧化应激水平影响的作用和机制。方法将大鼠分为5组,正常对照组、模型对照组、假手术组和两个实验组大鼠(分别每天灌胃5或20mg/kg番茄红素),15d后采用大脑中动脉栓塞法(MCAO)制备大鼠局灶性脑缺血/再灌注模型。分别在再灌注后第3h和第24h进行神经行为评分;再灌注24h后处死动物,计算脑梗死体积;测定脑组织一氧化氮(NO)、诱导型一氧化氮合酶(iNOS)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、丙二醛(MDA)及血清尿酸(UA)的含量及活性,并采用RT-PCR法检测脑皮质组织中低氧诱导因子(HIF)-1α mRNA、Bcl-2 mRNA的表达水平。结果与模型组比较,番茄红素组大鼠的脑梗死体积较小,神经症状较轻,脑组织SOD、CAT活性较高,iNOS活性及MDA、NO、血清UA的含量较低;与正常对照组相比,LP高剂量组HIF-1α mRNA表达上调;而Bcl-2 mRNA表达上调仅在LP低剂量组较为明显。结论番茄红素对大鼠的局灶性脑I/R损伤具有一定的保护作用,其机制可能与提高抗氧化酶活性,抑制脂质过氧化反应,降低iNOS活性,上调脑组织HIF-1α和Bcl-2水平有关。     

单核细胞趋化蛋白1 mRNA在新生鼠实验性缺氧缺血损伤脑组织中的表达

目的观察新生鼠实验性缺氧缺血性脑损伤（HIBD）后脑组织趋化因子单核细胞趋化蛋白1（MCP-1）mRNA的表达，探讨其在HIBD中的作用。方法采用结扎7d龄SD大鼠右侧颈总动脉并暴露于8％氧气环境2．5h，制作HIBD模型。采用TaqMan实时荧光定量逆转录聚合酶链反应，动态定量监测大脑皮质、海马区脑组织中MCP—1在HIBD后不同时间点表达的变化。假手术组为对照组。结果HIBD后6h右侧脑组织MCP-1 mRNA表达至高峰，显著高于对照组（P〈0．05）。12h组仍高于对照组（P〈0．05）。24h～72h降至接近对照组水平（P〉0．05）。结论HIBD后MCP-1 mRNA表达显著升高，推测MCP-1参与了缺氧缺血脑组织损伤的过程。     

雌激素对去势MCAO雌性大鼠Wnt信号通路的影响

目的:研究外源性雌激素对去势雌性大鼠大脑中动脉阻塞(MCAO)模型经典Wnt信号通路的影响,探讨雌激素在局灶性脑缺血中发挥神经保护作用的机制。方法:选取SPF级3个月龄Wistar雌性大鼠60只,采用去势雌性大鼠脑缺血模型,随机分为3组,假手术组、模型组、雌激素组[(17β-雌二醇,皮下注射,300μg/(kg·d)],每组20只。2,3,5-三苯基四唑氮红(TTC)染色法评估脑梗死体积,免疫组织化学、蛋白质印迹法测定左侧大脑皮质结肠腺瘤样息肉病(APC)蛋白和β-连环蛋白的表达。结果:雌激素组梗死体积[(255.43±51.43)mm3]比模型组[(490.75±93.38)mm3]小,2组差异有统计学意义(t=5.565,P=0.001)。免疫组织化学结果提示模型组APC蛋白表达水平高于其他2组,差异有统计学意义(均P0.05),雌激素组β-连环蛋白水平高于模型组(P0.05),与假手术组比较差异无统计学意义(P0.05)。蛋白质印迹法结果显示雌激素组APC蛋白表达低于模型组,β-连环蛋白的表达高于模型组,差异均有统计学意义(均P0.05)。结论:补充外源性雌激素可以通过下调皮质区APC蛋白表达,激活经典Wnt信号通路,进而发挥在去势雌性大鼠局灶性脑缺血损伤中的神经保护作用,为绝经激素治疗降低围绝经期妇女缺血性脑损伤的临床应用提供参考依据。     

黄芪总苷对大鼠脑缺血机制与前列腺素的关系

目的:研究黄芪总苷(astragalosides,AST)预处理的脑保护作用机制及其与前列腺素E2的关系.方法:采用间断静脉推注AST模拟预适应的实验方法,观察大鼠大脑中动脉栓塞再灌致脑梗死体积、血清中前列腺素E2(prostaglandin E2,PGE2)的含量的变化.结果:AST(20,40,80mg.kg-1)预处理明显减少脑梗塞体积、并可明显降低血清中PGE2含量.结论:黄芪总苷预处理对大鼠脑缺血再灌注损伤具有明显的保护作用,其机制与脑组织中减少PGE2的产生有密切的关系.     

眼针对大鼠脑缺血再灌注脑血流量及速度影响

目的观察眼针对脑缺血再灌注模型(CIRI)大鼠脑皮层血流量及流速影响,探讨眼针治疗脑缺血性疾病的可能机制。方法运用激光多普勒微循环测量仪检测缺血24 h模型大鼠大脑皮层组织血流量及血流速度;观察电镜下毛细血管管壁的结构变化。结果模型组与眼针组大鼠大脑皮层组织血流量与血流速度分别为(63.28±8.84)、(169.38±19.89) PU和(18.98±6.75)、(57.43±28.84) mm/s,与模型组比较,眼针组大鼠大脑皮层组织的血流量明显升高、血流速度明显加快(P<0.01);眼针组大鼠大脑皮层毛细血管的超微结构基本正常,模型组内皮细胞坏死、萎缩。结论眼针能够增加ICRI模型大鼠脑皮层组织血流量,提高血流速度,改善毛细血管的内皮细胞结构。     

银杏药质体对大鼠脑梗死保护作用的研究

目的研究银杏酮酯卵磷脂复合物（Complex EGb,C—EGb）对脑缺血损伤的保护作用。方法参照Zea Longa法制作大鼠大脑中动脉阻塞（MCAO）模型,测定其行为障碍和脑梗死范围。结果银杏酮酯卵磷脂复合物可见显著改善大鼠局灶性脑缺血所致的神经症状,明显减少脑梗死的体积。结论银杏酮酯卵磷脂复合物对脑缺血损伤具有较好的保护作用,效果优于等剂量（总黄酮）的杏灵颗粒和银杏磷脂混合物。     

丁基苯酞对大鼠脑缺血再灌注损伤后Bcl-2表达的影响

[目的]探讨丁基苯酞(NBP)对大鼠脑缺血再灌注损伤后Bcl-2蛋白和mRNA表达的影响。[方法]利用大脑中动脉线栓法将♂SD大鼠建立局灶性缺血再灌注模型,随机分为假手术组(不阻断大脑中动脉)、脑缺血再灌注组(I/R组)和NBP治疗组(NBP组),每组20只大鼠;脑缺血2h后开始再灌注。NBP组每天2次灌胃NBP,每次25mg/kg,I/R组及假手术组灌胃相同剂量食用植物油。再灌注72h后行神经功能缺损评分,然后断头取脑,TTC染色观察脑梗死体积,免疫组织化学(SP)方法检测梗死核心区、梗死周围区、海马区Bcl-2蛋白的表达,原位杂交方法(POD法)检测Bcl-2mRNA的表达。[结果]NBP组较I/R组大鼠脑梗死体积小(P﹤0.05),神经功能缺损改善(P﹤0.05);梗死核心区NBP组和I/R组Bcl-2蛋白和mRNA表达差异无统计学意义(P﹥0.05),梗死周围区和海马区NBP组Bcl-2蛋白和mRNA表达均高于I/R组和假手术组(P﹤0.05)。[结论]NBP减少脑缺血再灌注后大鼠脑梗死体积,改善神经功能,促进大鼠脑梗死周围区和海马区Bcl-2蛋白和mRNA的表达,可能为NBP抗凋亡和保护缺血脑组织的机制之一。