胃肠病学
胃腸病學
위장병학
CHINESE JOURNAL OF GASTROENTEROLOGY
2014年
11期
673-677
,共5页
孙晓萌%朱滢%王庆娥%柏建安%林琳
孫曉萌%硃瀅%王慶娥%柏建安%林琳
손효맹%주형%왕경아%백건안%림림
RhoA/ROCK信号通路%糖尿病%结肠动力障碍%免疫组织化学%印迹法,蛋白质
RhoA/ROCK信號通路%糖尿病%結腸動力障礙%免疫組織化學%印跡法,蛋白質
RhoA/ROCK신호통로%당뇨병%결장동력장애%면역조직화학%인적법,단백질
RhoA/ ROCK SignaIing Pathway%Diabetes MeIIitus%CoIon DysmotiIity%Immunohistochemistry%BIotting,Western
背景:糖尿病( DM)胃肠动力障碍的机制目前尚不明确,越来越多的研究认为胃肠平滑肌肌源性因素在该病的发生中起重要作用。近年RhoA/ROCK信号通路在DM并发症中的作用成为研究热点。目的:分析DM患者结肠肌层中RhoA/ROCK信号通路主要信号分子的表达变化,探讨该信号通路在DM结肠动力障碍中的可能作用。方法:收集2012年9月-2013年12月南京医科大学第一附属医院行结肠癌根治术患者的正常结肠组织,根据糖化血红蛋白水平,将患者分为DM组和对照组。采用免疫组化或蛋白质印迹法检测结肠肌层中RhoA/ROCK信号通路主要信号分子RhoA、ROCK1、MYPT1和p-MYPT1的表达情况。结果:免疫组化结果显示DM组结肠肌层中RhoA表达明显低于对照组,差异有统计学意义( P<0.05);蛋白质印迹法结果显示,与对照组相比,DM组RhoA、ROCK1和p-MYPT1蛋白表达均明显减少(0.62±0.42对1.15±0.69,0.54±0.09对0.75±0.05,0.70±0.28对1.04±0.47;P<0.05),而MYPT1蛋白表达差异无统计学意义(0.94±0.50对1.21±0.80,P>0.05)。结论:DM患者结肠肌层中RhoA/ROCK信号通路活性被抑制,可能与DM结肠动力障碍有一定相关性。
揹景:糖尿病( DM)胃腸動力障礙的機製目前尚不明確,越來越多的研究認為胃腸平滑肌肌源性因素在該病的髮生中起重要作用。近年RhoA/ROCK信號通路在DM併髮癥中的作用成為研究熱點。目的:分析DM患者結腸肌層中RhoA/ROCK信號通路主要信號分子的錶達變化,探討該信號通路在DM結腸動力障礙中的可能作用。方法:收集2012年9月-2013年12月南京醫科大學第一附屬醫院行結腸癌根治術患者的正常結腸組織,根據糖化血紅蛋白水平,將患者分為DM組和對照組。採用免疫組化或蛋白質印跡法檢測結腸肌層中RhoA/ROCK信號通路主要信號分子RhoA、ROCK1、MYPT1和p-MYPT1的錶達情況。結果:免疫組化結果顯示DM組結腸肌層中RhoA錶達明顯低于對照組,差異有統計學意義( P<0.05);蛋白質印跡法結果顯示,與對照組相比,DM組RhoA、ROCK1和p-MYPT1蛋白錶達均明顯減少(0.62±0.42對1.15±0.69,0.54±0.09對0.75±0.05,0.70±0.28對1.04±0.47;P<0.05),而MYPT1蛋白錶達差異無統計學意義(0.94±0.50對1.21±0.80,P>0.05)。結論:DM患者結腸肌層中RhoA/ROCK信號通路活性被抑製,可能與DM結腸動力障礙有一定相關性。
배경:당뇨병( DM)위장동력장애적궤제목전상불명학,월래월다적연구인위위장평활기기원성인소재해병적발생중기중요작용。근년RhoA/ROCK신호통로재DM병발증중적작용성위연구열점。목적:분석DM환자결장기층중RhoA/ROCK신호통로주요신호분자적표체변화,탐토해신호통로재DM결장동력장애중적가능작용。방법:수집2012년9월-2013년12월남경의과대학제일부속의원행결장암근치술환자적정상결장조직,근거당화혈홍단백수평,장환자분위DM조화대조조。채용면역조화혹단백질인적법검측결장기층중RhoA/ROCK신호통로주요신호분자RhoA、ROCK1、MYPT1화p-MYPT1적표체정황。결과:면역조화결과현시DM조결장기층중RhoA표체명현저우대조조,차이유통계학의의( P<0.05);단백질인적법결과현시,여대조조상비,DM조RhoA、ROCK1화p-MYPT1단백표체균명현감소(0.62±0.42대1.15±0.69,0.54±0.09대0.75±0.05,0.70±0.28대1.04±0.47;P<0.05),이MYPT1단백표체차이무통계학의의(0.94±0.50대1.21±0.80,P>0.05)。결론:DM환자결장기층중RhoA/ROCK신호통로활성피억제,가능여DM결장동력장애유일정상관성。
BacKground:The mechanism of diabetic gastrointestinaI dysmotiIity is stiII uncIear. More and more studies showed that gastrointestinaI smooth muscIe derived factors pIay an important roIe in gastrointestinaI dysmotiIity. RecentIy,the roIe of RhoA/ROCK signaIing pathway in diabetic compIications become a research hotspot. Aims:To investigate the possibIe roIe of RhoA/ROCK signaIing pathway in diabetic coIon dysmotiIity by examining the expressions of major signaIing moIecuIes in diabetic coIon muscIe. Methods:NormaI coIon tissue sampIes taken from patients undergoing radicaI surgery for coIonic cancer from Sept. 2012 to Dec. 2013 at the First AffiIiated HospitaI of Nanjing MedicaI University were coIIected. According to gIycated hemogIobin IeveI,the patients were divided into diabetes meIIitus( DM)group and controI group. The expressions of major signaIing moIecuIes in RhoA/ROCK1 signaIing pathway incIuding RhoA,ROCK1,MYPT1 and p-MYPT1 were determined by immunohistochemistry or Western bIotting. Results:Immunohistochemistry showed that expression of RhoA protein in DM group was significantIy Iower than that in controI group(P<0. 05). Western bIotting showed that expression IeveIs of RhoA,ROCK1 and p-MYPT1 proteins were significantIy Iower in DM group than in controI group(0. 62 ± 0. 42 vs. 1. 15 ± 0. 69,0. 54 ± 0. 09 vs. 0. 75 ± 0. 05,0. 70 ± 0. 28 vs. 1. 04 ± 0. 47;P<0. 05),whereas no significant difference in expression IeveI of MYPT1 protein was found between DM group and controI group(0. 94 ± 0. 50 vs. 1. 21 ± 0. 80,P>0. 05). Conclusions:The inhibition of RhoA/ROCK signaIing pathway in diabetic coIon muscIe may have some correIation with diabetic coIon dysmotiIity.