CAJ | 학술논문

目的：研究糖尿病大鼠模型的建立及其蛋白组学的变化，从蛋白质的分子水平上探索糖尿病发生的病理生理机制。方法：用高脂高糖饮食+链脲佐菌素的方法建立糖尿病大鼠模型，采用同位素标记技术，利用高效液相色谱仪及四级杆-静电场轨道阱质谱仪，对糖尿病大鼠进行串级质谱数据分析，对检测出的有统计学意义的表达差异蛋白进行研究。结果：第2周开始，模型组与正常组的血糖差异有统计学意义（P<0.05）。第10周，模型组血糖基本达到了糖尿病模型的标准，空腹血糖>16.7 mmol/L；蛋白组学检测共获得有显著差异的蛋白50个，其中上调大于1.5倍的蛋白17个，主要有MHCⅡ反式激活因子、主要尿蛋白、LIM结构域蛋白等；下调小于0.75倍的50个，主要有肉碱乙酰转移酶、多聚免疫球蛋白受体前体等。结论：建立了相对符合糖尿病发生发展规律的糖尿病大鼠模型，血清蛋白组学分析糖尿病发生的机制中存在免疫系统、糖代谢、脂代谢紊乱，从蛋白分子的水平研究糖尿病发生的病理生理基础，具有重要学术和临床意义。
목적：연구당뇨병대서모형적건립급기단백조학적변화，종단백질적분자수평상탐색당뇨병발생적병리생리궤제。방법：용고지고당음식+련뇨좌균소적방법건립당뇨병대서모형，채용동위소표기기술，이용고효액상색보의급사급간-정전장궤도정질보의，대당뇨병대서진행천급질보수거분석，대검측출적유통계학의의적표체차이단백진행연구。결과：제2주개시，모형조여정상조적혈당차이유통계학의의（P<0.05）。제10주，모형조혈당기본체도료당뇨병모형적표준，공복혈당>16.7 mmol/L；단백조학검측공획득유현저차이적단백50개，기중상조대우1.5배적단백17개，주요유MHCⅡ반식격활인자、주요뇨단백、LIM결구역단백등；하조소우0.75배적50개，주요유육감을선전이매、다취면역구단백수체전체등。결론：건립료상대부합당뇨병발생발전규률적당뇨병대서모형，혈청단백조학분석당뇨병발생적궤제중존재면역계통、당대사、지대사문란，종단백분자적수평연구당뇨병발생적병리생리기출，구유중요학술화림상의의。
Objective:To study the establishment of the diabetic rat models and the change of serum proteomics so as to exploring the pathophysiological mechanism of diabetes from the level of protein molecules. Methods:The diabetic rat models were established by streptozotocin(STZ)and high fat-glucose diet. The serum proteomics was analyzed with isotope internal standard dilution technique,high performance liquid chromatography/tandem mass spectrometry (LC-MS/MS). Results:From the second week,blood glucose in model group was significantly higher than that in normal group(P<0.05). For tenth week,the blood glucose of model group had basically reached the standard of diabetes model (FPG>16.7 mmol/L). There was significant difference in expression of 50 kinds of proteins between normal group and model group (17 kinds of proteins were up-regulated more than 1.5 times,including MHCⅡ transactivator,major urinary protein,LIM domain protein,etc;50 kinds of proteins down-regulated less than 0.75 times,including carnitine acetyltransferase,polymeric immunoglobulin receptor precursor,etc). Conclusion:The diabetic rat models were established successfully. Pathological mechanism of diabetes may be related to disorders of immune and glucolipid metabolism.