脑出血后多聚二磷酸腺苷核糖聚合酶过度表达与脑水肿的相关性

Objective To explore the mechanism of brain edema formation caused by hemoglobin after intracerebral hemorrhage (ICH). Methods Hemoglobin was infused into the right basal ganglia of SD rats with stereotactic guidance. The animals were killed 24 h later for detection of brain water and ion contents. Western blotting and immunohistochemistry were applied to detect the expression of poly( ADP-ribose) polymerase (PARP). The effect of the iron chelator deferoxamine ( DFX) on PARP expression was also examined. Results Intracerebral infusion of hemoglobin caused an increase in brain water content [from (78.7 ±0.3)% to (82. 1 ±1.2)% in ipsilateral basal ganglia] at 24th h. At the same time,PARP expression was up-regulated after hemoglobin infusion. By the intraperitoneal injection of 500 mg/kg DFX, brain edema induced by hemoglobin was attenuated significantly [from (82. 1 ±1.2)% to (80.4 ±1.0)% in ipsilateral basal ganglia] , and PARP expression was also down-regulated. Conclusion PARP might play a potential role, at least in part, in delayed edema development after ICH, and reducding iron production by iron chelator and down-regulating PARP overexpression might be a useful target for therapeutic intervention to limit brain edema after ICH.     

听神经鞘瘤术前评估指标与术后面神经功能保留的关系

目的探讨听神经鞘瘤术前评估与术后面神经功能保留的关系。方法对一组52例听神经鞘瘤术前按House-Brackmann面瘫量表分级,并根据头颅MRI对听神经鞘瘤大小进行分型,术后随访3个月,按House-Brackmann面瘫量表评估。结果 46例术后面神经功能得以保留,6例面神经功能未能保留,其中术前面瘫分级Ⅲ级2例,Ⅳ级4例;6例面神经功能未能保留中,MRI分型均为大型。结论 House-Brackmann面瘫分级和听神经鞘瘤MRI大小分型可以作为术前评估的临床指标,对术后面神经功能保留的判断有积极意义。     

脑出血后凝血酶诱导自噬细胞的种类研究

目的探讨脑出血后凝血酶诱导的自噬细胞类型。方法建立凝血酶脑损伤模型,大鼠脑内基底节注射凝血酶,收集脑损伤标本,免疫荧光双染检测beclin1~+与神经胶质纤维酸性蛋白(GFAP~+)以及神经元特异性烯醇化酶(NSE~+)的重合率;电镜下直接观察含有自噬泡的细胞。分别培养星形细胞和神经细胞,经凝血酶处理后,用Western blot法测量微管相关蛋白轻链3 (LC3)Ⅰ型向Ⅱ型转化,单丹磺酰戊二胺(MDC)染色观察细胞内自噬空泡的变化。结果大鼠基底节注射凝血酶后,免疫荧光双染显示beclin1+细胞主要为星形细胞;电镜显示,自噬空泡均位于星形细胞内,未能在神经细胞中发现。离体实验表明,凝血酶可以明显上调星形细胞中LC3Ⅱ/LC3Ⅰ比值,增加MDC染色标记的自噬空泡数量,神经细胞未见类似改变。结论脑出血后凝血酶诱导的细胞自噬主要发生于星形细胞,而不是神经细胞。     

脑出血后多聚二磷酸腺苷核糖聚合酶过度表达与脑水肿的相关性

目的 探讨血红蛋白导致脑出血(ICH)后脑水肿的机制.方法 将血红蛋白注入SD大鼠的右侧基底节区,24 h后将其处死取脑组织检测脑水含量及钠离子含量.同时,采用Western blot分析及免疫组织化学方法来检测多聚二磷酸腺苷核糖聚合酶(PARP)的表达,并观察铁螯合剂--去铁敏(DFX)对PARP表达的影响.结果 脑内注射血红蛋白后24 h发现注射侧脑水含量明显升高[基底节含水量由(78.7±0.3)%上升至(82.1±1.2)%],同时PARP表达上调;而在脑内注射血红蛋白同时腹腔注射500 mg/kg的去铁敏则能使PARP表达下调并且使脑水肿减轻[基底节含水量由(82.1±1.2)%降至(80.4±1.0)%].结论 在脑出血后血红蛋白诱导的迟发性脑水肿的形成过程中,PARP起到了潜在的重要作用;而螯合血红蛋白的降解产物铁并抑制PARP过度表达,有可能成为减轻脑出血后脑水肿的新的有效治疗方法.

Abstract：

Objective To explore the mechanism of brain edema formation caused by hemoglobin after intracerebral hemorrhage (ICH). Methods Hemoglobin was infused into the right basal ganglia of SD rats with stereotactic guidance. The animals were killed 24 h later for detection of brain water and ion contents. Western blotting and immunohistochemistry were applied to detect the expression of poly( ADP-ribose) polymerase (PARP). The effect of the iron chelator deferoxamine ( DFX) on PARP expression was also examined. Results Intracerebral infusion of hemoglobin caused an increase in brain water content [from (78.7 ±0.3)% to (82. 1 ±1.2)% in ipsilateral basal ganglia] at 24th h. At the same time,PARP expression was up-regulated after hemoglobin infusion. By the intraperitoneal injection of 500 mg/kg DFX, brain edema induced by hemoglobin was attenuated significantly [from (82. 1 ±1.2)% to (80.4 ±1.0)% in ipsilateral basal ganglia] , and PARP expression was also down-regulated. Conclusion PARP might play a potential role, at least in part, in delayed edema development after ICH, and reducding iron production by iron chelator and down-regulating PARP overexpression might be a useful target for therapeutic intervention to limit brain edema after ICH.     

凝血酶导致的星形细胞死亡中自噬激活以及作用研究

目的探讨凝血酶导致的星形细胞死亡中是否存在细胞自噬,以及自噬在此过程中的作用。方法孕21 d SD大鼠原代培养星形细胞分为:生理盐水组,凝血酶组(凝血酶处理),自噬抑制剂3-甲基腺嘌呤(3-MA)组(3-MA干预),凝血酶+3-MA组(凝血酶+3-MA共处理)。应用Western blot法检测微管相关蛋白轻链3(LC3)转化,免疫组化学染色检测beclin 1表达水平,单丹磺酰尸胺(MDC)染色观察细胞自噬空泡;乳酸脱氢酶(LDH)和活/死细胞计数评估细胞死亡。结果星形细胞经凝血酶处理24 h后,1LC3Ⅰ向LC3Ⅱ转化和beclin 1表达明显上升(P0.05)。2MDC染色示自噬空泡数显著增加;3-MA可降低LC3Ⅰ向LC3Ⅱ的转化,下调beclin 1表达(P0.01)和减少MDC染色自噬空泡(P0.05)。3细胞死亡检测,星形细胞经凝血酶处理后LDH水平和活/死细胞计数与生理盐水组比较,死亡细胞比例上升(均P0.05);3-MA干预后,LDH水平和活/死细胞计数中的死亡细胞比例较凝血酶组进一步上升(均P0.05)。结论凝血酶导致的星形细胞死亡过程中存在细胞自噬,抑制细胞自噬加重细胞死亡。     

磁共振成像T2*WI观察大鼠自发性脑出血含铁病灶的演变过程

目的:旨在研究用MRI T2*WI检测自发性脑出血后含铁病灶的演变过程.方法:大鼠脑内注射不同体积的自体动脉血(A组10μL;B组50μL;C组100μL).各组术后第1、3,7,14和30天行脑部MRI T2WI和T2*WI扫描,记录图像特征.由Image J软件进行图像分析.结果:大鼠脑内注射自体血后,MRI T2*WI图像较T2WI明显清晰;A、B组大鼠术后7和14 d含铁病灶体积T2*WI较T2WI所测得的体积更大(P<0.05); C组大鼠术后第7、14和30天,T2*WI比较T2WI测得的体积也更大(P<0.05).结论:在自发性脑出血后含铁病灶的检测中,MRI T2*WI较MRI T2WI更为清晰和敏感.     

磁共振成像T2~* WI检测在临床自发性脑出血含铁病灶演变过程中的应用

目的:旨在研究用磁共振成像(MRI)T2*WI检测临床自发性脑出血患者脑内含铁病灶的演变过程。方法:收集临床自发性脑出血患者10例,于发病后第1、7和14天行头颅MRIT1WI、T2WI、DWI和T2*WI系列扫描,记录图像特征,由Image J软件进行图像分析。结果:患者脑出血后MRI T2*WI序列显示的含铁病灶图像与其他MRI序列比较明显清晰;发病后第7和14天含铁病灶范围测量显示T2*WI序列比T2WI序列所测得的体积更大(P<0.05)。结论:住自发性脑出血脑内含铁病灶的检测中,MRI T2*WI序列较其他MRI序列图像更为清晰,与MRI T2WI相比也更为敏感。     

松果体实质细胞肿瘤治疗进展

松果体区实质细胞肿瘤病理跨度大,良性低度恶性的以手术为主,预后佳;中高度恶性以辅助治疗为主,预后差。手术、放疗、化疗、放射外科治疗各有优缺点和适应症,切除范围与预后关系不可忽视,肿瘤大小也影响治疗预后。     

CD47在小胶质细胞吞噬红细胞过程中的作用研究

目的 研究体外培养的小胶质细胞对红细胞的吞噬现象.探讨红细胞表面CD47表达变化对小胶质细胞吞噬红细胞的影响.方法 体外培养大鼠小胶质细胞.用PKH26标记红细胞后分为年轻红细胞组和衰老红细胞组,将标记好的红细胞加入培养的小胶质细胞中,用免疫荧光染色观察吞噬现象;用Western blot法分析年轻红细胞组与衰老红细胞组的CD47表达差异;用流式细胞仪对吞噬进行定量研究.结果 年轻红细胞组CD47表达较高,CD47/β-actin为(0.46±0.03);衰老红细胞组CD47表达明显降低,CD47/β-actin为(0.20±0.07),衰老红细胞的CD47表达降低>50%(P<0.05).衰老红细胞组较年轻红细胞组更容易被小胶质细胞吞噬(P<0.05).结论 红细胞表面CD47表达降低导致促进红细胞被小胶质细胞吞噬.     

脑出血后多聚二磷酸腺苷核糖聚合酶过度表达与脑水肿的相关性

Objective To explore the mechanism of brain edema formation caused by hemoglobin after intracerebral hemorrhage (ICH). Methods Hemoglobin was infused into the right basal ganglia of SD rats with stereotactic guidance. The animals were killed 24 h later for detection of brain water and ion contents. Western blotting and immunohistochemistry were applied to detect the expression of poly( ADP-ribose) polymerase (PARP). The effect of the iron chelator deferoxamine ( DFX) on PARP expression was also examined. Results Intracerebral infusion of hemoglobin caused an increase in brain water content [from (78.7 ±0.3)% to (82. 1 ±1.2)% in ipsilateral basal ganglia] at 24th h. At the same time,PARP expression was up-regulated after hemoglobin infusion. By the intraperitoneal injection of 500 mg/kg DFX, brain edema induced by hemoglobin was attenuated significantly [from (82. 1 ±1.2)% to (80.4 ±1.0)% in ipsilateral basal ganglia] , and PARP expression was also down-regulated. Conclusion PARP might play a potential role, at least in part, in delayed edema development after ICH, and reducding iron production by iron chelator and down-regulating PARP overexpression might be a useful target for therapeutic intervention to limit brain edema after ICH.