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81.
蛋白激酶C和蛋白酪氨酸激酶活性对缺血再灌注心肌细胞凋亡影响的实验研究 总被引:12,自引:1,他引:11
为探讨缺血预适应(Ischemic Preconditioning,IP)早期以及蛋白激酶C(Protein Kinase C,PKC)及蛋白酷氨酸激酶(Peotein Tyrosine Kinase,PTK)激动剂和抑制剂对缺血再灌注(I/R)心肌细胞凋亡的影响以及IP效能发挥通路中央PKC和PTK的关系。用TUNEL法检测I/R心肌细胞凋亡。结果显示:1、IP早期能显著降低I/R心肌细胞凋亡( 相似文献
82.
脑力智宝对PC12细胞缺血性损伤的保护作用 总被引:10,自引:0,他引:10
用NaCN加缺糖造成的PC12细胞缺血性损伤模型,研究脑力智宝含药血清对细胞的保护作用。并对所取含药血清时不同的给药次数,采血时间和含药血清加入量等实验方法进行了探讨。结果表明,单次给药后0.5、1.2、3h所采集的含药血清不具有细胞保护作用,而两次给药(间隔2h)后1h,2h的含药血清具有明显的保护作用。每日两次给经连续3.5d(7次给药)各时间点的含药血清均有明显的细胞保护作用。血清加入量以5 相似文献
83.
84.
K. Jendroska W. Poewe J. Pluess H. Iwerssen-Schmidt J. Paulsen S. Barthel L. Schelosky J. Cervós-Navarro S. E. Daniel S. J. DeArmond 《Acta neuropathologica》1995,90(5):461-466
The histoblot immunostaining technique for locating and characterizing amyloidogenic proteins was used to obtain information about the relationship of cerebral ischemia/hypoxia to the accumulation of amyloid protein (Aß). We investigated brains of 131 subjects (ages 25–94 years, mean 72 years). Three distribution patterns of A immunoreactivity were identified: (1) colocalization with diffuse and neuritic plaques of Alzheimer's disease (AD) and aging; (2) diffuse punctate deposits in the cerebral cortex in association with small vessel cerebral vascular disease; and (3) cerebral cortical accumulation localized to arterial boundary zones and other regions susceptible to ischemic/hypoxic injury designated stress-induced deposits (SID). SID were not identified in tissue sections by immunohistochemical, Congo red or Bielschowsky silver techniques; no histological abnormalities were present in adjacent formalin-fixed tissue sections. SID occurred in subjects with histories of cerebral ischemia, and severe orthostatic hypotension. There was also an association with aging in general and with the incidence of neuritic plaques specifically. These latter findings are consistent with the hypothesis that brain ischemia/hypoxia plays a role in the pathogenesis of AD. 相似文献
85.
发病72h内的急性缺血性脑梗死60例,分为2组。尼莫地平组30例(男性21例,女性9例;年龄59±s10a)。wk1.2给支持疗法(脱水剂,维生素C等)和尼莫地平2mg/d于5%葡萄糖液500ml内静脉滴注。wk3.4改用扩容、改善微循环,细胞活性药。wkl-4口服尼莫地平60mg.qn。对照组30例(男性23例,女性7例;年龄58±9a)。不给尼莫地平,其余同上。4wk后,前组神经功能缺损积分值较后组下降显著(P相似文献
86.
银杏叶提取物对兔心肌缺血再灌注损伤时中性粒细胞活化的影响 总被引:11,自引:0,他引:11
目的 观察兔心肌缺血再灌注前后PMN(中性粒细胞)的活性变化过程。了解银杏叶提取物保护心肌是否与影响中性粒细胞活化作用有关。方法 取30只日本大耳白兔随机均分为3组,假手术对照组、缺血再灌注组和实验用药组。用药方法:用自制的银杏叶提取物注射剂(总黄酮含量5mg/ml)5ml静滴给药。分别于冠脉结扎前和结扎缺血1h后采血用布式显微镜观察白细胞活化状态的变化。检测白细胞表面粘附分子CD11/CD18表 相似文献
87.
大鼠局灶性脑缺血神经细胞凋亡与坏死的研究 总被引:1,自引:1,他引:0
用凝胶电泳及原位末端标记研究大鼠脑缺血再灌流后神经元的凋亡与坏死。采用可逆性大脑中动脉阻塞2 小时,再灌流0.5~48 小时,造成脑缺血再灌流模型(30 只),用HE、原位末端标记(TUNEL)和琼脂糖凝胶电泳观察神经元的改变。结果:缺血损伤区位于视前区、纹状体和皮质,再灌流0.5 小时,视前区的缺血损伤区有较多的凋亡细胞,而皮质、纹状体仅有散在的凋亡细胞。再灌流3~6小时,凋亡细胞数量增多,并可见坏死细胞,12小时达高峰,持续到24 小时,并可见凋亡细胞各种形态,凋亡细胞主要位于缺血损伤区内界,坏死细胞也增多。48小时完全坏死区周围有成群的凋亡细胞。电泳显示涂片状背景上有明显的DNA带。细胞凋亡参与缺血再灌流所致的神经元损伤,凋亡细胞与坏死细胞并存,细胞凋亡使梗塞区面积扩大。 相似文献
88.
89.
Purpose. To investigate the role of phospholipase A2 (PLA2) in reperfusion injury of the kidney in an in vivo animal model, renal mitochondrial PLA2 activity was measured under three different conditions.
Methods. Male Wistar rats (n = 72) anesthetized with pentobarbital underwent renal ischemia surgically for 45 min and were reperfused for the indicated
time (renal ischemia/reperfusion). Treatments included reperfusion for various predetermined periods (phase 1), exposure to
hyperbaric oxygen (phase 2), and administration of reactive oxygen species (ROS) scavenger (phase 3). Thereafter, each kidney
was harvested, and mitochondrial PLA2 activity was measured by a radioisotope technique.
Results. Ischemia/reperfusion resulted in time-related PLA2 activation in the renal mitochondria up to 48 h of reperfusion after renal ischemia. Renal mitochondrial PLA2 activity was further augmented by hyperbaric oxygen exposure prior to reperfusion, whereas administration of the ROS scavengers
suppressed mitochondrial PLA2 activity.
Conclusion. These data suggest that ROS may play an important role in the in vivo activation of PLA2 associated with renal ischemia/reperfusion.
Received for publication on July 6, 1998; accepted on November 30, 1998 相似文献
90.
Effect of intracerebral norepinephrine depletion on outcome from severe forebrain ischemia in the rat 总被引:3,自引:0,他引:3
Nellgård BM Miura Y Burkhard Mackensen G Pearlstein RD Warner DS 《Brain research》1999,847(2):174-269
Manipulations of plasma catecholamine concentrations influence outcome from ischemic brain insults. It has been suggested that these effects are mediated by influences on brain catecholamine concentrations. This study examined whether major changes in brain norepinephrine concentrations can alter outcome from severe forebrain ischemia. Sprague-Dawley rats were administered 50 mg/kg i. p. N-(chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) or were left untreated (control). One week later, these rats were subjected to either 7 or 8 min of normothermic forebrain ischemia (bilateral carotid occlusion and MABP=30 mmHg) and allowed to recover for 4 days. Histologic damage was then evaluated. In other control and DSP-4-treated animals, hippocampal microdialysate norepinephrine concentrations were measured before, during and after 8 min of forebrain ischemia. Norepinephrine concentrations were also determined in brain homogenates from non-ischemic DSP-treated and control rats. A 95% depletion of norepinephrine was observed in brain homogenates from non-ischemic DSP-4-treated rats compared with control. During ischemia, microdialysate norepinephrine concentrations increased in control but not in DSP-4-treated rats (P=0.002). For plasma, intra-ischemic epinephrine concentrations increased 8-10-fold and returned to baseline values post-ischemia with no differences between groups. Plasma norepinephrine values remained unchanged in both groups. Histologic damage resulting from either 7 or 8 min of ischemia in hippocampal structures, caudoputamen, and neocortex was similar between DSP-4-treated and control groups. This study could not identify any effect of major changes in brain norepinephrine concentrations on ischemic brain damage. These data indicate that peripheral catecholamine effects on near-complete forebrain ischemic outcome are unlikely to be mediated by effects on central catecholamine concentrations. 相似文献