中国临床实用医学
中國臨床實用醫學
중국림상실용의학
CHINA CLINICAL PRACTICAL MEDICINE
2015年
3期
34-37
,共4页
王熙勋%姜立新%梁静%王景麟%翟慧渊%夏先明
王熙勛%薑立新%樑靜%王景麟%翟慧淵%夏先明
왕희훈%강립신%량정%왕경린%적혜연%하선명
急性胆道感染%细胞凋亡%BAX%BCL-2
急性膽道感染%細胞凋亡%BAX%BCL-2
급성담도감염%세포조망%BAX%BCL-2
Acute biliary tract infection%Apoptosis%BAX%BCL-2
目的:研究急性感染过程中是否存在肝细胞凋亡,并探讨肝细胞凋亡的可能机制。方法研究于2013年9至10月在烟台毓璜顶医院中心实验室进行。30只实验大鼠适应喂养7 d后随机分为5组,其中1组为对照组,余下4组为实验组,实验组通过胆总管注入大肠埃希菌,建立急性胆道感染模型,并于注入大肠埃希菌6、12、24及48 h后处死。对照组动物胆总管内注入1 ml生理盐水,6 h后处死。取各组肝组织,制作切片。TUNNEL染色,计数凋亡肝细胞;免疫组织化学试验检测BCL-2、BAX的表达。结果各实验组与对照组相比,TUNNEL染色阳性肝细胞表达差异有统计学意义(P<0.05),24 h和48 h组TUNNEL染色阳性表达较6 h组与12 h组明显增加(P<0.05)。对照组与实验组间BAX表达差异有统计学意义(P<0.05),随着时间延长表现出逐渐增多的趋势,但变化差异无统计学意义(P>0.05)。而BCL-2在对照组和6 h实验组间没有体现出明显差异,但随着时间的延长,以12 h与24 h组为界,实验组前后间的BCL-2表达出现显著差异。结论急性胆道感染后肝细胞在短时间内即会出现细胞凋亡,并且贯穿于急性胆道感染始终,基因层面表现为促凋亡基因BAX表达增强,抑制凋亡基因BCL-2表达减弱。且TUNNEL所示肝细胞凋亡改变与基因表达改变存在时间上的一致性,表明凋亡基因的改变可能带动了肝细胞凋亡的发生。
目的:研究急性感染過程中是否存在肝細胞凋亡,併探討肝細胞凋亡的可能機製。方法研究于2013年9至10月在煙檯毓璜頂醫院中心實驗室進行。30隻實驗大鼠適應餵養7 d後隨機分為5組,其中1組為對照組,餘下4組為實驗組,實驗組通過膽總管註入大腸埃希菌,建立急性膽道感染模型,併于註入大腸埃希菌6、12、24及48 h後處死。對照組動物膽總管內註入1 ml生理鹽水,6 h後處死。取各組肝組織,製作切片。TUNNEL染色,計數凋亡肝細胞;免疫組織化學試驗檢測BCL-2、BAX的錶達。結果各實驗組與對照組相比,TUNNEL染色暘性肝細胞錶達差異有統計學意義(P<0.05),24 h和48 h組TUNNEL染色暘性錶達較6 h組與12 h組明顯增加(P<0.05)。對照組與實驗組間BAX錶達差異有統計學意義(P<0.05),隨著時間延長錶現齣逐漸增多的趨勢,但變化差異無統計學意義(P>0.05)。而BCL-2在對照組和6 h實驗組間沒有體現齣明顯差異,但隨著時間的延長,以12 h與24 h組為界,實驗組前後間的BCL-2錶達齣現顯著差異。結論急性膽道感染後肝細胞在短時間內即會齣現細胞凋亡,併且貫穿于急性膽道感染始終,基因層麵錶現為促凋亡基因BAX錶達增彊,抑製凋亡基因BCL-2錶達減弱。且TUNNEL所示肝細胞凋亡改變與基因錶達改變存在時間上的一緻性,錶明凋亡基因的改變可能帶動瞭肝細胞凋亡的髮生。
목적:연구급성감염과정중시부존재간세포조망,병탐토간세포조망적가능궤제。방법연구우2013년9지10월재연태육황정의원중심실험실진행。30지실험대서괄응위양7 d후수궤분위5조,기중1조위대조조,여하4조위실험조,실험조통과담총관주입대장애희균,건립급성담도감염모형,병우주입대장애희균6、12、24급48 h후처사。대조조동물담총관내주입1 ml생리염수,6 h후처사。취각조간조직,제작절편。TUNNEL염색,계수조망간세포;면역조직화학시험검측BCL-2、BAX적표체。결과각실험조여대조조상비,TUNNEL염색양성간세포표체차이유통계학의의(P<0.05),24 h화48 h조TUNNEL염색양성표체교6 h조여12 h조명현증가(P<0.05)。대조조여실험조간BAX표체차이유통계학의의(P<0.05),수착시간연장표현출축점증다적추세,단변화차이무통계학의의(P>0.05)。이BCL-2재대조조화6 h실험조간몰유체현출명현차이,단수착시간적연장,이12 h여24 h조위계,실험조전후간적BCL-2표체출현현저차이。결론급성담도감염후간세포재단시간내즉회출현세포조망,병차관천우급성담도감염시종,기인층면표현위촉조망기인BAX표체증강,억제조망기인BCL-2표체감약。차TUNNEL소시간세포조망개변여기인표체개변존재시간상적일치성,표명조망기인적개변가능대동료간세포조망적발생。
Objective To determine whether liver cell apoptosis exist in the process of the acute infection, and to explore the possible mechanism of liver cell apoptosis. Methods 30 experimental rats were fed for 7 days and divided into 5 groups, one of them served as the model group, the other groups as the experimental group. The Escherichia coli were injected into the common bile duct of the four groups to establish the model of acute biliary. The four groups were sacrificed at 6, 12, 24 and 48h after injection of Escherichia coli. Injection of when the control group rats were injected 1 ml saline into the common bile duct and killed after 6h. Made sections with every rat’s’ liver tissue, counted apoptotic hepatocytes and detected the expression of BCL-2, BAX by immunohistochemistry chemical test methods. Results The expressions of the positive hepatocytes were significant differences between the model group and the experimental groups(P<0.05), also between 24、48 h and 6、12 h (P<0.05).BAX expression, There was a significantly different between the model group and the experimental groups on BAX expression , which gradually increased with time, but no significant difference change(P>0.05). There was not a significant difference between the model group and the 6h experimental group on BCL-2 expression, but BCL-2 expression is bounded 12 h and 24 h group, the experimental group between before and after the emergence of a significant difference. Conclusion Hepatocyte apoptosis appears in a short period of acute biliary tract infections, and throughout acute biliary tract infection, the expression on the gene level was to enhance the number of BAX and to decrease BCL-2. Changes in liver cell apoptosis and gene expression were in the consistency of the existence of time, indicating that changes in apoptotic gene led to the liver cell apoptosis.