CAJ | 학술논문

目的：在UCP2基因敲除小鼠中建立稳定的高血糖加重脑缺血再灌注损伤模型。方法KO-UCP2小鼠腹腔注射STZ诱导高血糖。大脑中动脉栓塞（MCAO）栓塞（1h）制备缺血模型，再灌注6，24，72h后分别运用HE染色和TTC染色观察缺血后细胞形态学和组织学损伤。结果高血糖组神经功能评分明显高于正常血糖组。HE染色显示，6h I/R组神经间质疏松，部分神经元变性、坏死。24h I/R组和72h IR组，核固缩神经细胞比例增加。高血糖组的核固缩神经细胞比率明显高于相应正常血糖组。TTC染色证实高血糖可以加重缺血后梗死面积。结论在KO-UCP2小鼠中建立高血糖加重脑缺血再灌注损伤模型的成功率、稳定性都有一定的提高，为进一步明确UCP2在高血糖加重脑缺血损伤中的作用奠定了基础。
목적：재UCP2기인고제소서중건립은정적고혈당가중뇌결혈재관주손상모형。방법KO-UCP2소서복강주사STZ유도고혈당。대뇌중동맥전새（MCAO）전새（1h）제비결혈모형，재관주6，24，72h후분별운용HE염색화TTC염색관찰결혈후세포형태학화조직학손상。결과고혈당조신경공능평분명현고우정상혈당조。HE염색현시，6h I/R조신경간질소송，부분신경원변성、배사。24h I/R조화72h IR조，핵고축신경세포비례증가。고혈당조적핵고축신경세포비솔명현고우상응정상혈당조。TTC염색증실고혈당가이가중결혈후경사면적。결론재KO-UCP2소서중건립고혈당가중뇌결혈재관주손상모형적성공솔、은정성도유일정적제고，위진일보명학UCP2재고혈당가중뇌결혈손상중적작용전정료기출。
Objective To investigate effects of mitochondrial uncoupling protein 2 on hyperglycemia -enhanced ischemic neuronal damage.Methods KO-UCP2 mice were randomly divided into two groups: hyperglycemia group and non- hyperglycemia group. Cerebral artery occlusion (MCAO) surgery was preparation for al KO-UCP2 mice. We treated al mice in according to the reperfusion of 6, 24, 72 hours. We evaluated models with using neurological deficits, and observed morphological changes of nerve cels with HE staining, and observed infarct size of mice’ brain with TTC staining.Results Higher score was significantly observed in hyperglycemia Group than non- hyperglycemia group at ZeaLonga Score evaluation. HE staining showed that there are nerve stroma osteoporosis, the neuron degeneration, apoptosis in 6h I/R group. In 24h and 72 I/R group, nucleus pycnosis neurons ratio was increased. TTC staining further confirmed that hyperglycemia can aggravate ischemic infarction area in KO-UCP2 mice.ConclusionThe higher success rate and clear symptoms were observed after hyperglycemia-aggravated cerebral Ischemia-reperfusion damage model in KO-UCP2 mice.