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新生鼠缺氧缺血性脑损伤脑组织S-100β蛋白、脑细胞内钙改变及尼莫地平的保护作用 被引量:5

The changes of S-100β protein and free calcium in brain of hypoxic-ischemic neonatal SD rats and the protective effect of nimodipine
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摘要 目的探讨新生鼠缺氧缺血性脑损伤(HIBD)脑组织S-100β蛋白、脑细胞内钙的改变及尼莫地平的神经保护作用。方法45只7日龄SD大鼠,采用随机区组设计分为尼莫地平治疗组、缺氧组及正常对照组。尼莫地平治疗组于HIBD模式后给予尼莫地平0.2 mg/(kg.d)+生理盐水2 ml,腹腔内注射,连续3 d,而缺氧组与正常对照组每天给予2 ml生理盐水腹腔内注射,连续3 d。三组分别于同一时间断头取脑。采用免疫组化法测定脑组织中S-100蛋白的含量,应用钙荧光指示剂Fura-ZAM法测定脑细胞胞浆游离钙离子浓度。结果缺氧组脑组织中S-100β蛋白阳性细胞数及细胞内钙含量均高于正常对照组(P<0.01),而尼莫地平治疗组上述指标均低于缺氧组(P<0.01),且与正常对照组比较差异均无统计学意义(P>0.05)。结论L-型钙离子通道阻滞剂尼莫地平能抑制新生鼠缺氧缺血性脑损伤S-100β蛋白及细胞内钙的释放,提示S-100β蛋白参与新生鼠HIBD,其机制可能与细胞内钙增高有关,尼莫地平具有神经保护作用。 Objective To explore the changes of S-100β protein and free calcium in brain of hypoxic- ischemic neonatal SD rats and the protective effect of nimodipine. Methods forty-five SD rats of 7 days old were randomly divided into three groups: nimodipine-treated group, hypoxic-ischemic group and normal control group. In nimodipine-treated group, the rats were given nimodipine intraperitoneally for 3 days in doses of 0.2 mg/( kg· d) with 2 ml nattri sodium soon after the HIE model was performed. In hypoxia-isehemia group, the rats were given nattri sodium in same dose intraperitoneally for 3 days after the HIE model was performed , and the rats were treated with pseudo operation in normal group and were given nattri sodium of same dose and period. All the rats were decapitated after 3 days and the S-100β protein in cerebral tissue were detected by immnohistochemical method, and the concentration of free calcium in brain cells were measured by calcium fluorescence indicator in Fura-ZAM. Results The levels of S-100 β protein and free calcium in hyponic-ischemic group were obviously higher than that of nimodipine-treated group and normal control group (P 〈 0. 01), wheneas there were not significante differente between nimodipine-treated group and control group( P 〉 0.05). Conclusion Nimodipine can inhibited the release of S-100 β protein in hypoxic-isehemis cerebral cell and prevent calcium influx;S-100 β protein may be invloved in the cause of cerebral hypoxie-isehemic injury and related to the increase of free calcium, which may reveal nimodipine nerval protective function.
出处 《中国小儿急救医学》 CAS 2006年第1期14-16,共3页 Chinese Pediatric Emergency Medicine
基金 广东省湛江市科技攻关项目(030908)
关键词 新生鼠 缺氧缺血性脑损伤 S-100Β蛋白 细胞内游离钙 尼莫地平 Neonatal rats Hypoxic-ischemic brain damage S-100β protein Intracellular free calcium Nimodipine
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