CAJ | 학술논문

目的：观察糖尿病大鼠胸主动脉组织形态学及平滑肌钙激活钾通道（Ca2+-activated K+channels, KCa）表达的变化。方法采用高糖高脂饲料喂养SD大鼠8周和链脲佐菌素腹腔注射（30 mg/kg）建立实验性糖尿病大鼠模型，检测血液生化指标，进行胸主动脉HE、弹力纤维、Masson染色和抗平滑肌α-actin免疫组织化学染色，并采用逆转录聚合酶链反应和免疫印迹技术观察主动脉平滑肌KCa通道表达的变化。结果与年龄匹配的对照组大鼠相比，模型大鼠体质量下降，血糖、血脂、糖化血红蛋白和平均血压明显升高，并出现多食、多饮、多尿等典型糖尿病体征；主动脉组织学出现早期粥样硬化变化，表现为内皮受损不完整，表面有炎细胞粘附，内膜下平滑肌细胞排列紊乱，局部增生，弹力纤维中断、融合，胶原纤维增多等；主动脉中层平滑肌KCa1.1α亚单位和β亚单位表达降低，KCa3.1表达明显增加。结论平滑肌KCa表达转换参与糖尿病动脉粥样硬化的发生。
목적：관찰당뇨병대서흉주동맥조직형태학급평활기개격활갑통도（Ca2+-activated K+channels, KCa）표체적변화。방법채용고당고지사료위양SD대서8주화련뇨좌균소복강주사（30 mg/kg）건립실험성당뇨병대서모형，검측혈액생화지표，진행흉주동맥HE、탄력섬유、Masson염색화항평활기α-actin면역조직화학염색，병채용역전록취합매련반응화면역인적기술관찰주동맥평활기KCa통도표체적변화。결과여년령필배적대조조대서상비，모형대서체질량하강，혈당、혈지、당화혈홍단백화평균혈압명현승고，병출현다식、다음、다뇨등전형당뇨병체정；주동맥조직학출현조기죽양경화변화，표현위내피수손불완정，표면유염세포점부，내막하평활기세포배렬문란，국부증생，탄력섬유중단、융합，효원섬유증다등；주동맥중층평활기KCa1.1α아단위화β아단위표체강저，KCa3.1표체명현증가。결론평활기KCa표체전환삼여당뇨병동맥죽양경화적발생。
Objective To investigate the changes in aorta morphology and Ca2+-activated K+ (KCa) channel expression in the diabetic rats. Methods A diabetic rat model was established by a single intraperitoneal injection of streptozotocin (30 mg/kg) after a modified high fat and glucose diet for 8 weeks. Pathological changes in the aorta were observed with HE staining, elastic fiber staining, Masson's trichrome staining and immunohistochemistry. Both the mRNA and protein levels of KCa channels in the aorta were measured by RT-PCR and Western blotting. Results Early atherosclerotic changes were observed in the aorta wall of the diabetic rats. The mRNA and protein levels of KCa1.1 channel α- and β-subunits were significantly decreased, while the expression of KCa3.1 channels was obviously enhanced in the middle layer of the aorta in the diabetic rats. Conclusion KCa channel switching in smooth muscles may play a role in the development of atherosclerosis in diabetic rats.