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作 者:舒泉[1] 陈蒙华[2] 王慧慧[1] 阮氏芳英 谢露[1]
机构地区:[1]广西医科大学基础医学院生理教研室,南宁530021 [2]广西医科大学第一附属医院心内科,南宁530021
出 处:《基因组学与应用生物学》2016年第8期1871-1876,共6页Genomics and Applied Biology
基 金:国家自然科学基金资助项目(81160231)资助
摘 要:探究p38通路在心肺复苏后大鼠脑组织过氧化物岐化酶(superoxide dismutase,SOD)表达过程中的作用以及对脑细胞凋亡的影响。经食道交流电刺激诱导心室颤动(VF)建立大鼠心脏骤停/心肺复苏(cardiac arrest/cardiopulmonary resuscitation,CA/CPR)模型。假手术(SH)组大鼠只行手术操作,不诱导CA/CPR(n=6)。恢复自主循环后的48只大鼠随机分成两组,分别为SKF86002(SKF)组(2.5 mg/kg,iv.,n=24)和模型组(给予等量生理盐水,n=24),每组分别设12 h、24 h、48 h、72 h四个检测时间点,每个时间点6只大鼠。用免疫荧光标记法检测大脑皮层过氧化物岐化酶的荧光密度,TUNEL标记法检测细胞凋亡情况。结果发现:CPR后,SKF组在各时间点的SOD1和SOD2的荧光密度均较模型组较高(p<0.05)。但是CPR后72 h,SKF组的凋亡率明显较模型组高(p<0.05)。表明SKF干预治疗能显著提高心脏骤停/心肺复苏后模型大鼠脑组织的SOD的表达水平,但并不能抑制脑细胞凋亡。This essay is written to explore effects of P38 signal pathways activate on the expression of antioxidant enzymes and the apoptosis of brain tissue in rats. That uses the alternating current via the esophagus stimulation to induce ventricular fibrillation and establish cardiac arrest/cardiopulmonary resuscitation (CA/CPR) model. Sham group (SH) was treated without CA/CPR (n=6). Forty-eight rats, once spontaneous circulation was restored, were randomly divided into two groups, SKF86002 (SKF) group (2.5 mg/kg, iv., n=24) and model group (inject equal of normal saline, n=24). Each group seted four detection points at 12 h, 24 h, 48 h, 72 h respectively; at each time, six rats were taken. The brain tissue of superoxide dismutase fluorescence density was detected with immunofluore- scence labeling method and the apoptosis rate was detected with TUNEL labeling method. After CPR, the SOD fluorescence density of SKF group was higher than that of the model group (P〈0.05); But after 72h ofCPR, apoptosis rate of SKF group was obviously higher than that of the model group (P〈0.05). This research showed that SKF86002 could improve the SOD's expression, but it could not inhibit cell apoptosis in rat's brain tissue after cardiac arrest.
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