沙土鼠全脑适应性再灌注的脑保护机制研究

目的动态研究不同灌注时间和灌注量对全脑组织缺血损害的恢复程度和即早基因c- fos的表达,以探明适应性再灌注的脑保护作用机制.方法沙土鼠随机分7组,实验组夹闭两侧颈总动脉,造成沙土鼠全脑缺血模型,夹闭10 min后,不同开放时间段(4 min,8 min,10 min,15 min,30 min)开放不同脑血流量(1/4,1/2,一次性全开放)和单纯血液稀释后分别观察缺血海马CA区c-fos蛋白的表达,及缺血区大脑半球的改善状况.结果开放15 min,1/2脑血流量时c-fos蛋白表达最高(P<0.05),海马CA区缺血损害改善最明显,开放15 min,全脑血流量一次性开放时海马CA区损害最严重.结论①在适应性灌注流量中,脑缺血海马区c-fos的表达和神经元凋亡呈反相作用关系;②低流量灌注有明显改善脑缺血的作用;③夹闭10 min后,开放1/2脑血流量,持续15 min的效果比一次性再灌注开放效果要好.     

沙土鼠全脑缺血适应性再灌注脑保护的凋亡机制研究

脑梗塞、重度脑外伤或外伤性脑血管病、颈内动脉狭窄介入治疗一次性再灌注再通时易致脑血管收缩功能紊乱，引起脑灌注压突破致脑组织再灌注损伤。控制性低流量再灌注可以减轻一次性再灌注损伤，有较好的脑保护作用。脑适应性再灌注（adapted reperfusion，AR）是全新的再灌注观念，是相对于一次性再灌注而言的灌注方法，它将再灌注量和时机的动态观念引入缺血一再灌注损伤的机制及治疗研究之中，即在血液稀释的基础上，进一步控制灌注的量，改一次性灌注为控制性灌注，     

巴曲酶用药次数对脑缺血再灌注沙土鼠脑保护作用的影响

目的 研究巴曲酶用药次数对脑缺血再灌注(IR)沙土鼠脑保护作用的影响.方法 沙土鼠45只,随机分为IR模型组、正常组、巴曲酶3次用药组(3次组)、5次用药组(5次组)和7次用药组(7次组).采用双侧颈总动脉夹闭5 min后再通建立沙土鼠脑IR损伤模型.3次组、5次组、7次组均在造模成功后腹腔注射巴曲酶(8 BU/kg),隔日1次,分别给药3次、5次、7次;IR模型组和正常组腹腔注射等量的生理盐水,共7次.用流式细胞仪检测各组沙土鼠海马区凋亡细胞数,电镜观察海马CA1区细胞形态.结果 巴曲酶3次组、5次组和7次组海马区凋亡细胞数显著少于IR组(均P＜0.05);5次组海马区凋亡细胞数明显少于3次组(P＜0.05),而5次组与7次组之间差异无统计学意义(P＞0.05);正常组仅有极少凋亡细胞.5次组细胞超微结构改变要轻于3次组,与7次组相比无明显差异.结论 巴曲酶3次、5次和7次用药均可减少脑IR后神经元的凋亡;但5次和7次用药的脑保护作用明显好于3次用药.     

硫酸镁对大鼠脑缺血-再灌注损伤的脑保护研究

目的：观察ＭｇＳＯ４作为非竞争性ＮＭＤＡ－Ｒ拮抗剂对大鼠脑缺血－再灌注的保护作用。方法：用线栓法制作７２只Ｗｉｓｔａｒ大鼠的大脑中动脉栓塞模型,在术后２小时给予再灌注,分别在再灌注同时及其２小时后给予不同剂量ＭｇＳＯ４治疗,术后进行皮层脑电图描记,测定血Ｍｇ＾２＋浓度,进行运动功能评估,测定脑组织含水量,观察病理组织学变化,并计算凋亡细胞数。结果：ＭｇＳＯ４能减少扩展性抑制波产生数目（Ｐ〈０．０５）;１０％,ＭｇＳＯ４组疗效优于５％ＭｇＳＯ４组,并明显改善大鼠运动功能,且早期给药效果更佳（Ｐ〈０．０５）;ＭｇＳＯ４能减轻脑组织含水量;但在短期内不能减少凋亡细胞数。结论：通过电生理、病理研究和临床评估证明ＭｇＳＯ４对大鼠脑缺血－再灌注损伤确有保护作用。     

沙土鼠全脑缺血再灌注损伤的实验研究

比较暂时单次阻断和分次阻断动脉所致脑缺血损伤的严重程度.24只雄性沙土鼠经双侧颈总动脉阻断脑缺血模型,分单次阻断10min组与阻断5min,灌注10min,再阻断5min.24h后断头取脑行抗微管相关蛋白2(MAP2)免疫组化染色,计算机图像分析系统行病变范围测定.分次阻断组动物的海马下脚CA1区及额顶叶脑皮层Ⅲ～Ⅳ层缺血性损伤程度比单次长时间阻断减少了2.04%,但两者比较无明显的统计学差异(P>0.05).分次阻断间歇期行再灌注能否加重脑缺血损伤的程度主要受分次阻断的强度、阻断持续时间、再灌注时间的长短以及个体的脑血管侧支循环能力而定.     

吡硫醇对沙土鼠脑缺血和再灌注能量代谢的影响

用沙土鼠制成缺血及再灌注模型，观察到在缺血５０ｍｉｎ时脑能量代谢明显障碍，再灌注３０ｍｉｎ时有所改善，而在再灌注１２０ｍｉｎ时发生迟发性能量代射恶化。吡硫醇（脑复新）可明显改善缺血５０ｍｉｎ时的能量代谢，并能纠正再灌注１２０ｍｉｎ时的迟发性能量代谢恶化。本文讨论吡硫醇对脑损伤保护作用的机制。     

阿司匹林对沙土鼠全脑缺血-再灌注后脑内一氧化氮合酶及一氧化氮的影响

目的观察阿司匹林对沙土鼠全脑缺血-再灌注后的脑保护作用及其与脑内一氧化氮合酶及一氧化氮水平变化的关系。方法采用夹闭双侧颈总动脉的方法,制备沙土鼠短暂性全脑缺血-再灌注模型。27只健康雄性蒙古沙土鼠随机分为假手术组、脑缺血-再灌注组和阿司匹林治疗组,观察缺血7min再灌注24h后沙土鼠脑组织的病理学改变,以及一氧化氮合酶与一氧化氮水平的变化。结果病理学检查结果显示,沙土鼠脑缺血7min再灌注24h后海马CA1区缺血性损害明显,脑组织内一氧化氮合酶及一氧化氮水平显著升高(P<0.01);与脑缺血-再灌注组相比,阿司匹林治疗组沙土鼠的病理损害较轻,一氧化氮合酶与一氧化氮水平明显下降(P<0.01)。结论阿司匹林可显著减轻脑缺血-再灌注后的脑损伤,其作用机制可能与抑制一氧化氮合酶与一氧化氮水平上升有关。     

硒对沙土鼠脑缺血再灌注损伤后MDA、GSH-PX及细胞凋亡的影响

目的 研究亚硒酸钠对沙土鼠脑缺血再灌注损伤的保护作用及其机制。方法 将50只沙土鼠随机分为5组，Ⅰ组：假手术组；Ⅱ组：缺血再灌注1天处死组；Ⅲ组：缺血再灌注4天处死组；Ⅳ组：硒处理、缺血再灌注1天处死组；Ⅴ组：硒处理、缺血再灌注4天处死组。采用夹闭双侧颈动脉法制备沙土鼠脑缺血再灌注模型，焦油紫染色，光镜下观察各组海马CAl区神经细胞的形态变化，TUNEL染色观察神经细胞凋亡情况，计算凋亡密度。同时测定脑组织中丙二醛(MDA)、谷胱甘肽过氧化酶(GSH-PX)的含量。结果硒处理组沙土鼠缺血再灌注后，光镜下病理形态损伤较轻，凋亡密度较小，GSH-PX含量较高。结论 硒对沙土鼠脑缺血再灌注损伤具有保护作用，其机制可能与增强脑缺血再灌注早期脑组织中GSH-PX的活性，抑制氧自由基损伤，减轻脂质过氧化反应，而减轻缺血再灌注后细胞的坏死和凋亡有关。     

沙鼠全脑适应性再灌注c-fos表达的实验研究

目的动态研究不同灌注时间和灌注量对全脑组织缺血损害的恢复程度和即早基因。c-fos的表达,以探明适应性再灌注的脑保护作用机制。方法沙鼠随机分7组,实验组夹闭两侧颈总动脉,造成沙土鼠全脑缺血模型,夹闭10 min后,不同开放时问段(4 min,8 min,10 min,15 min,30 min),开放不同脑血流量(1/ 4,1/2,一次性全开放)和单纯血液稀释后分别观察缺血海马CA区c-fos蛋白的表达,及缺血区大脑半球的改善状况。结果开放15 min,1/2脑血流量时c-fos蛋白表达最高(P<0.05),海马CA区缺血损害改善最明显,开放15 min,全脑血流量一次性开放时海马CA区损害最严重。结论(1)在适应性灌注流量中,脑缺血海马区c-fos的表达和神经元凋亡呈反相作用关系;(2)低流量灌注有明显改善脑缺血的作用,夹闭10min后, 开放1/2脑血流量,持续15 min的效果比一次性再灌注开放效果要好。     

不同剂量巴曲酶对脑缺血沙土鼠的脑保护作用

目的　探讨巴曲酶对脑缺血沙土鼠脑保护作用的最佳剂量。方法　80只沙土鼠随机分为假手术组、对照组、巴曲酶治疗组(又分为1BU/kg、2BU/kg、4BU/kg、8BU/kg、16BU/kg、32BU/kg组),每组10只。制作完全性前脑缺血再灌注沙土鼠模型,制作模型前3h给予对照组沙土鼠腹腔注射生理盐水;巴曲酶组腹腔注射相应剂量的巴曲酶。用原位末端标记(TUNEL)法染色检测沙土鼠海马CA1 区凋亡细胞,光镜下计算海马CA1 区的神经元凋亡率。结果　巴曲酶8BU/kg、16BU/kg、32BU/kg组海马CA1 区细胞凋亡率明显减少,与对照组及巴曲酶1BU/kg、2BU/kg、4BU/kg组比较差异有显著性(均P<0. 01), 8BU/kg、16BU/kg、32BU/kg组之间差异无显著性(均P>0 .05)。结论　巴曲酶具有抗脑缺血后的细胞凋亡作用;巴曲酶8BU/kg为对脑缺血沙土鼠脑保护作用的最佳剂量。     

大蒜素对全脑缺血再灌注损伤大鼠海马凋亡相关蛋白表达的影响

目的观察大蒜素对全脑缺血再灌注损伤大鼠海马凋亡相关蛋白表达的影响,进一步探讨大蒜素的脑保护机制。方法雄性Wistar大鼠30只,随机分为5组:假手术组(Sham组);缺血再灌注组(IR组);缺血再灌注+大蒜素10 mg/kg(All-10 mg)、20 mg/kg(All-20 mg)、30 mg/kg(All-30 mg)组,夹闭两侧颈总动脉8 min再灌注24 h建立大鼠全脑缺血再灌注模型,取海马组织硫堇染色观察海马组织学改变及存活神经元密度;免疫组织化学染色测定海马CA1区Bcl-2、Bax蛋白的表达。结果与Sham组相比,IR组海马CA1区神经元密度明显降低,Bax蛋白表达明显增加(均P0.05);与IR组相比,大蒜素处理各组海马CA1区神经元密度明显增多,Bcl-2蛋白表达明显增加,Bax蛋白表达明显减少,其中以All-20 mg组变化最显著(均P0.05)。结论大蒜素可以通过影响凋亡相关蛋白的表达而抑制细胞凋亡,从而发挥脑保护作用。     

An optimal dose of tea polyphenols protects against global cerebral ischemia/reperfusion injury

Previous studies addressing the protection of tea polyphenols against cerebral ischemia/ reperfusion injury often use focal cerebral ischemia models, and the optimal dose is not unified. In this experiment, a cerebral ischemia/reperfusion injury rat model was established using a modified four-vessel occlusion method. Rats were treated with different doses of tea polyphenols (25, 50, 100, 150, 200 mg/kg) via intraperitoneal injection. Results showed that after 2, 6, 12, 24, 48 and 72 hours of reperfusion, peroxide dismutase activity and total antioxidant capacity in brain tissue gradually increased, while malondialdehyde content gradually decreased after tea polyphenol intervention. Tea polyphenols at 200 mg/kg resulted in the most apparent changes. Terminal deoxynucleotidyl transferase-mediated nick end labeling and flow cytometry showed that 200 mg/kg tea polyphenols significantly reduced the number and percentage of apoptotic cells in the hippocampal CA1 region of rats after cerebral ischemia/reperfusion injury. The open field test and elevated plus maze experiments showed that tea polyphenols at 200 mg/kg strengthened exploratory behavior and reduced anxiety of cerebral ischemia/reperfusion injured rats. Experimental findings indicate that tea polyphenols protected rats against cerebral ischemia/ reperfusion injury and 200 mg/kg is regarded as the optimal dose.     

Changes in neuronal apoptosis and apoptosis modulatory factors in cerebral ischemia/reperfusion

BACKGROUND: The high concentration of glutamate release is the main cause for neuronal cell death. The relationship between glutamate level and apoptosis during ischemia/reperfusion injury is still unclear. OBJECTIVE: To observe the neuronal apoptosis at 24 and 72 hours following cerebral ischemia/reperfusion in rats, and analyze the possible influencing factors. DESIGN: A randomized controlled animal experiment. SETTING: School of Medicine, Southern Yangtze University. MATERIALS: Totally 30 male adult Sprague Dawley (SD) rats of clean grade, weighing 240–290 g, were obtained from Shanghai Experimental Animal Center, Chinese Academy of Sciences. The rats were randomly divided into sham-operated group (n=10) and model group (n=20). Each group was observed at 24 and 72 hours after ischemia/reperfusion, 5 rats at each time point in the sham-operated group, whereas 12 at 24 hours and 8 at 72 hours in the model group. Kits for determining apoptosis and Bcl-2 were bought from Wuhan Boster Biological Technology, Co., Ltd.; Kit for calcineurin from Nanjing Jiancheng Bioengineering Institute. METHODS: The experiment was carried out in the Functional Scientific Research Room of Southern Yangtze University from June to October in 2006. ① Right middle cerebral artery was occluded by inserting a thread through internal carotid artery (ICA). The surgical process for the sham-operated rats was the same as that in the model group except a nylon suture inserted the ICA. According to Longa five-degree standard, the neurological deficit evaluation of rats was evaluated after surgery, and grades 1–3 were taken as successful model establishment. The blood was recirculated by withdrawing the nylon filament under anesthesia at 2 hours after ischemia in successful rat models. ②After reperfusion, the brain tissue was quickly removed at 24 or 72 hours and the slices were obtained from optic chiasma to funnel manubrium. The changes of the number of apoptotic cells were observed using the terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeling method. The expressions of Bcl-2 protein were determined with immunohistochemical staining. The activity of calcineurin was determined by the inorganic phosphorus method. The content of excitatory amino acid was detected by high performance liquid chromatography. MAIN OUTCOME MEASURES: ① Glutanate content in brain tissue; ② Conditions of apoptosis; ③ Calcineurin activity in brain tissue; ④ Bcl-2 expression in brain tissue. RESULTS: Totally 30 SD rats were used, 5 died and the other 25 were involved in the analysis of results. ① Changes of apoptosis: There were 0–3 apoptotic cells in the sham-operated group. In the model group, the numbers of apoptotic cells were obviously increased at 24 and 72 hours of reperfusion (P < 0.01), and it was markedly reduced at 72 hours as compared with 24 hours (P < 0.01). ② Changes of glutanate content: The glutamate contents at 24 and 72 hours of reperfusion in the model group were obviously higher than those in the sham-operated group (P < 0.01); In the model group, it was obviously increased at 24 hours as compared with 72 hours (P < 0.01). ③ Changes of Bcl-2 protein: In the model group, the Bcl-2 protein expression had no obvious changes at 24 hours of reperfusion, and it was obviously enhanced at 72 hours, which was obviously different from that in the sham-operated group and that at 24 hours (P < 0.01). ④ Changes of calcinerin activity: In the model group, the activity of calcineurin in brain tissue had no obvious changes at 24 hours of reperfusion; The activity of calcineurin at 72 hours was obviously higher than that in the sham-operated group and that at 24 hours (P < 0.01). CONCLUSION: The brain cyto-apoptosis action at different time points following reperfusion incompletely depends on the glutamate levels, while it depends on the interaction of some apoptosis related factors, such as amino acid, calcineurin, and Bcl-2, etc.     

Triptolide for cerebral ischemia/reperfusion injuryt

BackgroundStudies have demonstrated that triptolide has good anti-inflammatory and immunosuppressive effects. However, the effect of triptolide on cerebral ischemia/reperfusion injury is still unclear.ObjectiveTo observe the effects of triptolide on neurologic function, infarct volume, water content of brain tissue, neutrophil number in microvascular wall and interleukin-1β(IL-1β) expression in rat models of local ischemia/reperfusion, and analyze the mechanism of triptolide for protecting brain.DesignRandomized controlled experiment.SettingDepartment of Pathology, Medical School of Ningbo University; Department of Forensic Medicine, Tongji Medical College of Huazhong University of Science and Technology.MaterialsSixty Wistar rats of either gender, aged 4 months old, weighing from 200 to 250 g, were provided by the Experimental Animal Center, Tongji Medical College, Huazhong University of Science and Technology. Triptolide was purchased from Fujian Institute for Medical Science (purity 99.98%; Batch No. 2000215). It was dissolved in 20 g/L propanediol, and filtered with 200-mesh filter for later use.MethodsThis experiment was carried out in the laboratory of Forensic Medicine, Tongji Medical College of Huazhong University of Science and Technology, Department of Pathology, Medical School of Ningbo University between January 2001 and September 2004.

Sixty Wistar rats were randomized into 4 groups: sham-operation group, model group, low-dose triptolide group and high-dose triptolide group. Rats in each group, except for sham-operation group, were developed into rat models of cerebral ischemia/reperfusion according to the method of Longa et al. In the first 3 days of modeling, rats in the low- and high-dose triptolide groups were intraperitoneally injected with 0.2 and 0.4 mg/kg triptolide respectively, once a day, 3 days in total.

At ischemia 1 hour and reperfusion 24 hours, infarct volume, neurologic deficit (five-point scale, higher scores indicated poor neurologic function), water content of brain tissue, neutrophil number in microvascular wall in the middle cerebral artery occlusive side of rats were detected, meanwhile, brain tissue injury degree and IL-1βimmunohistochemical staining changes in brain-derived nerve cells were observed under the optical microscope.Main outcome measuresNeurologic deficit, infarct volume percentage, water content of brain tissue, neutrophil number in microvascular wall and positive rate of IL-1β immunoreaction.ResultsSixty rats were all involved in the final analysis.

Neurologic deficit scores of rats in the low- and high-dose triptolide groups were (1.96±0.14) and (1.75±0.16)points respectively, which were both significantly lower than those in model group [(2.58±0.11)points,P < 0.05,0.01].

Infarct volume percentages of rats in low- and high-dose triptolide groups were significantly lower than that in model group separately (P < 0.05, 0.01).

Water content of brain tissue of rats in model group was significantly higher than that in the sham-operation group [(82.35±1.26)% vs. (76.65±1.17)%,P < 0.01]; Water content of brain tissue of rats in the low- and high-dose triptolide groups was respectively(80.15±1.43)%,(78.23± 1.15)%, which was significantly lower than that in the model group (P < 0.05, 0.01).

Pathological changes of brain tissue of rats: Under the optical microscope, infarct focus was not found in the brain tissue of rats in the sham-operation group, while clear infarct focus could be found in the brain tissue of rats in the model group; Although infarct focus was found in the brain tissue of rats in the low- and high-dose triptolide groups, the whole infarct area was contracted as compared as that in the model group.

Neutrophil number in microvascular wall of brain tissue of rats in the low- and high dose triptolide groups was 10.60±2.12,8.11±1.21 respectively, which was significantly less than that in model group(16.25±1.96,P < 0.05,0.01).

Positive rate of IL-1βimmunoreaction in the brain tissue of rats in model group was significantly higher than that in the sham-operation group (P < 0.01); and positive rate of IL-1β immunoreaction in the brain tissue of rats in low- and high-dose triptolide groups was significantly lower than that in the model group (P < 0.05, 0.01), but higher than that in the sham-operation group, without significant difference (P > 0.05).ConclusionTriptolide protects against cerebral ischemia/reperfusion injury of rats that may be related with anti-inflammations. Triptolide inhibits IL-1β expression in brain tissue and reduces the attachment and aggregation of neutrophils in blood capillary, and further inhibits the infiltration of blood white cells, thus, it will lessen cerebral injury, contract cerebral infarct and improve cerebral function.     

Triptolide for cerebral ischemia/reperfusion injury

BACKGROUND: Studies have demonstrated that triptolide has good anti-inflammatory and immunosuppressive effects. However, the effect of triptolide on cerebral ischemia/reperfusion injury is still unclear. OBJECTIVE: To observe the effects of triptolide on neurologic function, infarct volume, water content of brain tissue, neutrophil number in microvascular wall and interleukin-1β(IL-1β) expression in rat models of local ischemia/reperfusion, and analyze the mechanism of triptolide for protecting brain. DESIGN: Randomized controlled experiment. SETTING: Department of Pathology, Medical School of Ningbo University; Department of Forensic Medicine, Tongji Medical College of Huazhong University of Science and Technology. MATERIALS: Sixty Wistar rats of either gender, aged 4 months old, weighing from 200 to 250 g, were provided by the Experimental Animal Center, Tongji Medical College, Huazhong University of Science and Technology. Triptolide was purchased from Fujian Institute for Medical Science (purity 99.98%; Batch No. 2000215). It was dissolved in 20 g/L propanediol, and filtered with 200-mesh filter for later use. METHODS: This experiment was carried out in the laboratory of Forensic Medicine, Tongji Medical College of Huazhong University of Science and Technology, Department of Pathology, Medical School of Ningbo University between January 2001 and September 2004. ① Sixty Wistar rats were randomized into 4 groups: sham-operation group, model group, low-dose triptolide group and high-dose triptolide group. Rats in each group, except for sham-operation group, were developed into rat models of cerebral ischemia/reperfusion according to the method of Longa et al. In the first 3 days of modeling, rats in the low- and high-dose triptolide groups were intraperitoneally injected with 0.2 and 0.4 mg/kg triptolide respectively, once a day, 3 days in total. ② At ischemia 1 hour and reperfusion 24 hours, infarct volume, neurologic deficit (five-point scale, higher scores indicated poor neurologic function), water content of brain tissue, neutrophil number in microvascular wall in the middle cerebral artery occlusive side of rats were detected, meanwhile, brain tissue injury degree and IL-1βimmunohistochemical staining changes in brain-derived nerve cells were observed under the optical microscope. MAIN OUTCOME MEASURES: Neurologic deficit, infarct volume percentage, water content of brain tissue, neutrophil number in microvascular wall and positive rate of IL-1β immunoreaction. RESULTS: Sixty rats were all involved in the final analysis. ① Neurologic deficit scores of rats in the low- and high-dose triptolide groups were （1.96±0.14） and （1.75±0.16）points respectively , which were both significantly lower than those in model group [（2.58±0.11）points，P < 0.05，0.01]. ② Infarct volume percentages of rats in low- and high-dose triptolide groups were significantly lower than that in model group separately (P < 0.05, 0.01). ③Water content of brain tissue of rats in model group was significantly higher than that in the sham-operation group [（82.35±1.26）% vs. （76.65±1.17）%，P < 0.01]; Water content of brain tissue of rats in the low- and high-dose triptolide groups was respectively（80.15±1.43）%，（78.23± 1.15）%, which was significantly lower than that in the model group (P < 0.05, 0.01). ④Pathological changes of brain tissue of rats: Under the optical microscope, infarct focus was not found in the brain tissue of rats in the sham-operation group, while clear infarct focus could be found in the brain tissue of rats in the model group; Although infarct focus was found in the brain tissue of rats in the low- and high-dose triptolide groups, the whole infarct area was contracted as compared as that in the model group. ⑤Neutrophil number in microvascular wall of brain tissue of rats in the low- and high dose triptolide groups was 10.60±2.12，8.11±1.21 respectively, which was significantly less than that in model group（16.25±1.96，P < 0.05，0.01）. ⑥Positive rate of IL-1βimmunoreaction in the brain tissue of rats in model group was significantly higher than that in the sham-operation group (P < 0.01); and positive rate of IL-1β immunoreaction in the brain tissue of rats in low- and high-dose triptolide groups was significantly lower than that in the model group (P < 0.05, 0.01), but higher than that in the sham-operation group, without significant difference (P > 0.05). CONCLUSION: Triptolide protects against cerebral ischemia/reperfusion injury of rats that may be related with anti-inflammations. Triptolide inhibits IL-1β expression in brain tissue and reduces the attachment and aggregation of neutrophils in blood capillary, and further inhibits the infiltration of blood white cells, thus, it will lessen cerebral injury, contract cerebral infarct and improve cerebral function.     

短暂脑缺血再灌流后ATP含量变化与细胞凋亡的关系

目的:探讨短暂脑缺血再灌流后能量的动态变化及其与细胞凋亡之间的关系。方法:采用线栓法建立大鼠大脑中动脉闭塞(MCAO)模型,缺血10min后于再灌流后0h、1h、3h、6h、12h、24h和72h应用毛细血管电泳法分别测定额顶叶皮质的ATP含量,同时采用荧光显微镜、流式细胞仪和脱氧核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测细胞凋亡情况,分析两者之间的关系。结果:缺血10min后额顶叶皮质ATP的含量急剧下降至对照组的20%。再灌流后ATP的含量逐渐恢复,于再灌流后1h、3h、6h和12h恢复至对照组的70.5%、65.7%、84.8%和86.9%。再灌流后24hATP含量再次下降,再灌流后24h和72hATP含量仅为对照组的50%,与对照组相比差异有统计学意义(P<0.01和0.05)。缺血10min再灌流24h额顶叶皮质开始出现细胞凋亡现象,并随着时间延长凋亡细胞数目逐渐增加。结论:短暂脑缺血再灌流后大鼠额顶叶皮质存在细胞能量系统功能恢复滞后的现象和继发性细胞能量系统功能衰竭的现象,其中继发性细胞能量系统功能衰竭现象与细胞凋亡之间可能存在互为因果的关系。     

神经节苷脂对大鼠脑缺血再灌注损伤的脑保护作用

目的探讨神经节苷脂对大鼠脑缺血再灌注损伤的脑保护作用。方法采用线栓法制作缺血再灌注大鼠模型,分别用神经节苷脂(治疗组)和生理盐水(对照组)腹腔注射。观察两组大鼠缺血90min、缺血90min再灌注24h的脑梗死面积、神经功能缺损程度、细胞凋亡数、细胞凋亡率。结果治疗组大鼠于相同时间点脑梗死面积较对照组明显减小,仅表现轻度的神经功能缺损,且神经细胞的凋亡数较对照组显著减少(均P<0.01)。结论神经节苷脂能明显减小大鼠实验性脑缺血的脑梗死面积,减轻脑缺血再灌注后神经功能缺损程度,显著减轻缺血区神经元损害,具有显著的脑保护作用。