CAJ | 학술논문

目的观察宫内发育迟缓新生大鼠胰腺中Nkx2.2和Nkx6.1的表达。方法研究时间为2012年6月至2014年12月。清洁级Wistar 大鼠，低蛋白饮食法建立宫内发育迟缓（IUGR）模型，摘取胰腺组织，称重，应用免疫组织化学法检测新生大鼠胰腺组织中Nkx2.2和Nkx6.1的表达。结果 IUGR 组新生大鼠胰腺组织重量显著低于对照组（P<0.05）。与对照组相比，IUGR 组胰腺表现为组织松散，胰岛面积减少，胰腺中Nkx6.1的表达明显低于对照组（P<0.05）。IUGR 组 Nkx2.2的表达面积低于对照组，光密度值略低于正常组，但差异无统计学意义（P>0.05）。结论 IUGR 组Nkx6.1表达影响胰腺的发育，这可能是导致IUGR 大鼠成年期易罹患糖尿病的原因之一，对其进行深入研究将为新生儿胰腺功能发育障碍及先天性糖尿病的分子机制研究提供新的理论依据，并为开发新生儿胰腺功能发育障碍及先天性糖尿病的靶向药物提供了潜在的临床靶标。
목적관찰궁내발육지완신생대서이선중Nkx2.2화Nkx6.1적표체。방법연구시간위2012년6월지2014년12월。청길급Wistar 대서，저단백음식법건립궁내발육지완（IUGR）모형，적취이선조직，칭중，응용면역조직화학법검측신생대서이선조직중Nkx2.2화Nkx6.1적표체。결과 IUGR 조신생대서이선조직중량현저저우대조조（P<0.05）。여대조조상비，IUGR 조이선표현위조직송산，이도면적감소，이선중Nkx6.1적표체명현저우대조조（P<0.05）。IUGR 조 Nkx2.2적표체면적저우대조조，광밀도치략저우정상조，단차이무통계학의의（P>0.05）。결론 IUGR 조Nkx6.1표체영향이선적발육，저가능시도치IUGR 대서성년기역리환당뇨병적원인지일，대기진행심입연구장위신생인이선공능발육장애급선천성당뇨병적분자궤제연구제공신적이론의거，병위개발신생인이선공능발육장애급선천성당뇨병적파향약물제공료잠재적림상파표。
Objective To investigate the expression of Nkx2.2 and Nkx6.1 in pancreas of rats with intrauterine growth restriction(IUGR). Methods From June 2012 to December 2014,Rats were treated with low protein fodder from 1st day to delivery to create IUGR model.The removed pancreas of the rats measured weight. then,immunohistochemisty staining was performed to detect the expression of Nkx2.2 and Nkx6.1 in pancreas of rats. Results Stattistically significant reduction of the pancreatic weight were observed in IUGR group(P<0.05).Lower expression of Nkx 6.1 was observed in IUGR group (P<0.05).The expression of Nkx2.2 is slightly reduced,but they did not achieve statistical significance (P>0.05). Cluclusion Nkx6.1 expression in IUGR may impact the development of pancreas,which may be one of the reason that IUGR rats are easier to get Diabetes mellitus II in adulthood,Its in-depth study will provide a new theoretical basis for the newborn pancreas molecular mechanism of developmental disorders and congenital diabetes, and provide a potential target for the development of clinical neonatal pancreatic developmental disorders and congenital diabetes drug targeting .