中国基层医药
中國基層醫藥
중국기층의약
CHINESE JOURNAL OF PRIMARY MEDICINE AND PHARMACY
2014年
6期
801-802
,共2页
史玉%王建华%李青梅%郭永泽%李校天
史玉%王建華%李青梅%郭永澤%李校天
사옥%왕건화%리청매%곽영택%리교천
胰腺炎%锌指蛋白A20%Toll样受体4
胰腺炎%鋅指蛋白A20%Toll樣受體4
이선염%자지단백A20%Toll양수체4
Pancreatitis%Zinc finger protein A20%Toll-like receptor 4
目的 研究锌指蛋白A20对大鼠急性重症胰腺炎LPS-TLR4信号通路的影响.方法 采用5％牛磺胆酸钠溶液胰胆管注射诱发急性重症胰腺炎(SAP)大鼠模型,24只大鼠按数字表法随机分为三组.A组(假手术组)、B组(SAP模型组)、C组(SAP+ LPS组),每组8只.免疫组织化学法检测胰腺组织TLR4、NF-κBp65和p38MAPK的水平.结果 与A组相比,B、C组胰腺组织中锌指蛋白A20表达明显下降(t=17.234、19.698,均P＜0.05),而TLR4、NF-κBp65和p38MAPK表达均明显增加(t=15.909、20.432、16.543、18.629、22.105、19.006,均P＜0.05).C组与B组相比锌指蛋白A20表达明显下降(t=14.894,P＜0.05),而TLR4、NF-κBp65和p38MAPK表达均明显增加(t=14.047、15.582、17.070,均P＜0.05).结论 SAP时胰腺锌指蛋白A20的表达减少,对LPS-TLR4通路的抑制作用减弱,使胰腺损伤加重.
目的 研究鋅指蛋白A20對大鼠急性重癥胰腺炎LPS-TLR4信號通路的影響.方法 採用5％牛磺膽痠鈉溶液胰膽管註射誘髮急性重癥胰腺炎(SAP)大鼠模型,24隻大鼠按數字錶法隨機分為三組.A組(假手術組)、B組(SAP模型組)、C組(SAP+ LPS組),每組8隻.免疫組織化學法檢測胰腺組織TLR4、NF-κBp65和p38MAPK的水平.結果 與A組相比,B、C組胰腺組織中鋅指蛋白A20錶達明顯下降(t=17.234、19.698,均P＜0.05),而TLR4、NF-κBp65和p38MAPK錶達均明顯增加(t=15.909、20.432、16.543、18.629、22.105、19.006,均P＜0.05).C組與B組相比鋅指蛋白A20錶達明顯下降(t=14.894,P＜0.05),而TLR4、NF-κBp65和p38MAPK錶達均明顯增加(t=14.047、15.582、17.070,均P＜0.05).結論 SAP時胰腺鋅指蛋白A20的錶達減少,對LPS-TLR4通路的抑製作用減弱,使胰腺損傷加重.
목적 연구자지단백A20대대서급성중증이선염LPS-TLR4신호통로적영향.방법 채용5％우광담산납용액이담관주사유발급성중증이선염(SAP)대서모형,24지대서안수자표법수궤분위삼조.A조(가수술조)、B조(SAP모형조)、C조(SAP+ LPS조),매조8지.면역조직화학법검측이선조직TLR4、NF-κBp65화p38MAPK적수평.결과 여A조상비,B、C조이선조직중자지단백A20표체명현하강(t=17.234、19.698,균P＜0.05),이TLR4、NF-κBp65화p38MAPK표체균명현증가(t=15.909、20.432、16.543、18.629、22.105、19.006,균P＜0.05).C조여B조상비자지단백A20표체명현하강(t=14.894,P＜0.05),이TLR4、NF-κBp65화p38MAPK표체균명현증가(t=14.047、15.582、17.070,균P＜0.05).결론 SAP시이선자지단백A20적표체감소,대LPS-TLR4통로적억제작용감약,사이선손상가중.
Objective To investigate the effects of the zinc finger protein A20 on LPS-TLR4 signaling pathways in severe acute pancreatitis(SAP) rats.Methods 24 SD rats were randomly divided into 3 groups:group A(the sham operation group),group B (the SAP group),group C (the SAP group treated with LPS).SAP model was induced by retro-injection of intraductal 5％ sodium taurocholate into the biliary-pancreatic duct as previously described.The protein expression of A20,TLR4,NF-κBp65 and p38MAPK in pancreatic tissues was evaluated by immunohistochemistry.Results The positive area of A20 in pancreatic tissues was decreased in group B and group C compared with that in group A (t =17.234,19.698,all P ＜ 0.05).On the contrary,the expression of TLR4,NF-κBp65 and p38MAPK in pancreatic tissues were up-regulated(t =15.909,20.432,16.543,18.629,22.105,19.006,all P ＜ 0.05).A20 was decreased in group C than that in group B (t =14.894,P ＜ 0.05),while TLR4、NF-κBp65 and p38MAPK were increased in group C than those in group B (t =14.047,15.582,17.070,all P ＜0.05).Conclusion The expression of A20 reduced and TLR4,NF-κBp65 and p38MAPK enhanced in the pancreas of rats with SAP,which indicated that A20 inhibited LPS-TLR4 signaling pathways which play important roles in the pathogenesis of SAP.
