中国生化药物杂志
中國生化藥物雜誌
중국생화약물잡지
CHINESE JOURNAL OF BIOCHEMICAL PHARMACEUTICS
2014年
3期
40-43
,共4页
抗心磷脂抗体%细胞外信号调节蛋白激酶1/2%流产%母胎界面%安子合剂
抗心燐脂抗體%細胞外信號調節蛋白激酶1/2%流產%母胎界麵%安子閤劑
항심린지항체%세포외신호조절단백격매1/2%유산%모태계면%안자합제
anticardiolipin antibodies%ERK1/2%abortion%maternal-fetal interface%Anziheji
目的：研究细胞外信号调节蛋白激酶（extracellular signal regulated kinase，ERK）1/2信号通路参与抗心磷脂抗体（anticardiolipin antibodies，ACA）阳性流产的发病过程，从细胞增殖的角度阐明安子合剂对ERK1/2信号通路的影响。方法采用免疫组化方法检测ACA阳性流产模型组、空白对照组、安子合剂低/中/高剂量组和阿司匹林组小鼠母胎界面ERK1、ERK2磷酸化水平。结果 JD801形态学统计分析结果显示安子合剂低剂量组ERK1平均光密度值（0.678±0.097）接近空白对照组的平均光密度值（0.727±0.047），差异无统计学意义；模型组、安子合剂中剂量组、高剂量组、阿司匹林组ERK1平均光密度值（0.434±0.066、0.613±0.041、0.487±0.061、0.551±0.056）均较空白对照组明显降低，差异均有统计学意义（P＜0.01）。模型组、安子合剂低剂量组、中剂量组、高剂量组、阿司匹林组ERK2平均光密度值（0.430±0.058、0.621±0.041、0.562±0.047、0.449±0.062、0.515±0.045）均较空白对照组（0.708±0.038）明显降低，差异有统计学意义（P＜0.01）。结论安子合剂可以通过ERK信号转导通路提高细胞增殖的活性，改善胎盘功能，改变妊娠结局。
目的：研究細胞外信號調節蛋白激酶（extracellular signal regulated kinase，ERK）1/2信號通路參與抗心燐脂抗體（anticardiolipin antibodies，ACA）暘性流產的髮病過程，從細胞增殖的角度闡明安子閤劑對ERK1/2信號通路的影響。方法採用免疫組化方法檢測ACA暘性流產模型組、空白對照組、安子閤劑低/中/高劑量組和阿司匹林組小鼠母胎界麵ERK1、ERK2燐痠化水平。結果 JD801形態學統計分析結果顯示安子閤劑低劑量組ERK1平均光密度值（0.678±0.097）接近空白對照組的平均光密度值（0.727±0.047），差異無統計學意義；模型組、安子閤劑中劑量組、高劑量組、阿司匹林組ERK1平均光密度值（0.434±0.066、0.613±0.041、0.487±0.061、0.551±0.056）均較空白對照組明顯降低，差異均有統計學意義（P＜0.01）。模型組、安子閤劑低劑量組、中劑量組、高劑量組、阿司匹林組ERK2平均光密度值（0.430±0.058、0.621±0.041、0.562±0.047、0.449±0.062、0.515±0.045）均較空白對照組（0.708±0.038）明顯降低，差異有統計學意義（P＜0.01）。結論安子閤劑可以通過ERK信號轉導通路提高細胞增殖的活性，改善胎盤功能，改變妊娠結跼。
목적：연구세포외신호조절단백격매（extracellular signal regulated kinase，ERK）1/2신호통로삼여항심린지항체（anticardiolipin antibodies，ACA）양성유산적발병과정，종세포증식적각도천명안자합제대ERK1/2신호통로적영향。방법채용면역조화방법검측ACA양성유산모형조、공백대조조、안자합제저/중/고제량조화아사필림조소서모태계면ERK1、ERK2린산화수평。결과 JD801형태학통계분석결과현시안자합제저제량조ERK1평균광밀도치（0.678±0.097）접근공백대조조적평균광밀도치（0.727±0.047），차이무통계학의의；모형조、안자합제중제량조、고제량조、아사필림조ERK1평균광밀도치（0.434±0.066、0.613±0.041、0.487±0.061、0.551±0.056）균교공백대조조명현강저，차이균유통계학의의（P＜0.01）。모형조、안자합제저제량조、중제량조、고제량조、아사필림조ERK2평균광밀도치（0.430±0.058、0.621±0.041、0.562±0.047、0.449±0.062、0.515±0.045）균교공백대조조（0.708±0.038）명현강저，차이유통계학의의（P＜0.01）。결론안자합제가이통과ERK신호전도통로제고세포증식적활성，개선태반공능，개변임신결국。
Objective To study the role of ERK1/2 signaling pathways on the process of ACA positive abortion and explore the effect of Anziheji on ERK1/2 signaling pathways from cell proliferation.Methods Levels of ERK1/2 on maternal-fetal interface of every mice in ACA positive abortion model group,blank control group,Anziheji low,mediate,high dose group,aspirin group were detected by immunohistochemical. Results The average optical density value of ERK1 in Anziheji low dose group(0.678 ±0.097)was close to normal group(0.727 ±0.047),there was no significant difference between them.Compared with blank control group,the ERK1 average optical density value in model group(0.434 ±0.066),Anziheji dose group(0.613 ±0.041),high dose group(0.487 ±0.061)and aspirin group(0.551 ±0.056)were significantly lower,and the differences were all statistically significant(P<0.01).Compared with blank control group(0.708 ±0.038),the ERK2 average optical density values in model group(0.430 ±0.058), Anziheji low dose group(0.621 ±0.041),mediate dose group(0.562 ±0.047),high dose group(0.449 ±0.062)and aspirin group(0.515 ±0.045) were significantly lower,and the differences were all statistically significant (P <0.01 ).Conclusion Anziheji can improve the activity of cell proliferation,improve the function of the placenta and change the outcome of pregnancy through ERK signal pathway.
