樊永梅，张长杰，彭文娜，尹婧，徐睿，胡治平.无热量超短波治疗对大鼠脑缺血再灌注损伤后SPCA1的影响[J].中华物理医学与康复杂志,2018,40(1):11-14
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| 无热量超短波治疗对大鼠脑缺血再灌注损伤后SPCA1的影响 |
| The influence of ultra-shortwave irradiation on Ca2+-ATPase expression after cerebral ischemia and reperfusion |
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| DOI： |
| 中文关键词: 脑缺血再灌注 大脑中动脉栓塞 SPCA1 高尔基体应激 超短波 |
| 英文关键词: Cerebral ischemia Reperfusion MCAO/R SPCA1 Golgi apparatus stress Ultra-short waves |
| 基金项目:国家自然科学基金（81171239） |
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| 中文摘要: |
| 目的 观察无热量超短波治疗对大鼠脑细胞缺血再灌注损伤后脑梗死体积、分泌途径衍生钙离子转运ATP酶（Secretory-pathway Ca2+-ATPase，SPCA）1的影响。 方法 选取80只SD大鼠，将大鼠分为假手术组（8只）、模型组（36只）、超短波组（36只）。用线栓法制备一侧大脑中动脉栓塞再灌注大鼠模型，模型组和超短波组大鼠进行造模处理，假手术组大鼠处理同模型组和超短波组，但不插入线栓。模型组按照再灌注时间分为模型1d组（12只）、模型3d组（12只）、模型7d组（12只），超短波治疗组分为超短波1d组（12只）、超短波3d组（12只）、超短波7d组（12只）。各亚组分别于造模后1d、3d、7d处死取标本。用红四氮唑染色法观察并计算每组大鼠的脑梗死体积，采用Western blot法检测患侧海马SPCA1蛋白变化。 结果 假手术组大鼠脑切片均红染，未见梗死灶。缺血再灌注后，模型组和超短波组大鼠脑缺血区域出现白色梗死灶，随着时间延长，脑梗死体积均减小。与模型组同时间点比较，超短波组脑梗死体积均较小（P<0.05）。与假手术组比较，除超短波7d组外，各组大鼠SPCA1均降低 (P<0.05)。随着时间延长，模型组和超短波组大鼠SPCA1增加(P<0.05)。与模型组同时间点比较，超短波1d组大鼠SPCA1轻度增加，但差异无统计学意义（P>0.05），超短波3d组、超短波7d组大鼠SPCA1较模型组3d组、模型组7d组显著增加，差异有统计学意义（P<0.05）。 结论 无热量超短波治疗可减小脑梗死体积，减轻脑缺血再灌注损伤，其机制可能是抑制了SPCA1表达水平下调，从而减轻了神经细胞凋亡，促进神经功能恢复。 |
| 英文摘要: |
| Objective To observe the influence of ultra-shortwave (USW) irradiation on infarct volume and Ca2+-ATPase (SPCA) secretion after brain ischemia and reperfusion. Methods Eighty Sprague-Dawley rats were randomly divided into a sham operation group (n=8), a model group (n=36) and a USW group (n=36). The animal model of middle cerebral artery ischemia and reperfusion (MCAO/R) was established using the suture method in the rats of the model and USW groups, while the sham operation group was given the same operation but without inserting the thread plug. One day, 3 days and 7 days after the intervention, 12 rats were sacrificed and the infarct volumes and SPCA1 protein expression were measured using 2,3,5-triphenyltetrazolium chloride staining and western blotting. Results No white infarcted tissue was found in the sham operation group. In the model and USW groups the volume of infarcted tissue decreased with time. Significantly less infarcted volume was observed in the USW group compared to the model group at each time point. The SPCA1 levels in the brain tissue were lower than in the sham operation group after one and 3 days of USW treatment, but they were significantly lower in the model group as well. As time went by, the average SPCA1 level increased significantly in the model and USW groups. A slightly higher SPCA1 level was observed in the USW group compared to the model group after one day of treatment, but with no significance. However, significant differences were found between them after 3 and 7 days of intervention. Conclusion Ultra-shortwave irradiation can protect against MCAO/R injury by decreasing the infarcted volume, which may be related to down-regulation of SPCA1, minimizing nerve cell apoptosis and promoting neural functional recovery, at least in rats. |
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