全科医学临床与教育
全科醫學臨床與教育
전과의학림상여교육
Clinical Education of General Practice
2015年
5期
500-503
,共4页
P38丝裂原活化蛋白激酶%肝脏缺血再灌注损伤
P38絲裂原活化蛋白激酶%肝髒缺血再灌註損傷
P38사렬원활화단백격매%간장결혈재관주손상
p38MAPK%liver ischemia reperfusion injury
目的:探讨P38丝裂原活化蛋白激酶(p38MAPK)特异性活性抑制剂(FR167653)对大鼠肝脏缺血再灌注损伤保护作用的机理。方法利用封闭群SD大鼠肝脏部分缺血再灌注模型,将实验动物分假手术组、对照组、治疗组。分别在各个时间点按照相应程序采集标本检测肝组织髓过氧化物酶(MPO)活性、免疫组化检测黏附分子表达及肝组织诱生型一氧化氮合酶iNOS mRNA表达测定。结果肝脏缺血再灌注损伤后,对照组肝脏组织中MPO活性增高,而治疗组肝脏组织MPO活性明显低于对照组(t分别=3.30、3.10、4.10、2.90,P均<0.05);同时在治疗组中炎性趋化因子的表达也较对照组明显减低(t分别=3.70、4.30、4.60、4.90、3.50、4.00,P均<0.05)。免疫组化结果显示对照组肝组织内可见P-选择素(P-selectin)及细胞间黏附分子-1(ICAM-1)在肝组织中表达,而治疗组表达阳性率明显低于对照组;iNOS的mRNA表达水平在3 h和6 h时治疗组明显低于对照组(t分别=4.50、5.70,P均<0.05)。结论 FR167653能在多个环节、多个层次对缺血再灌注肝脏起着保护作用。
目的:探討P38絲裂原活化蛋白激酶(p38MAPK)特異性活性抑製劑(FR167653)對大鼠肝髒缺血再灌註損傷保護作用的機理。方法利用封閉群SD大鼠肝髒部分缺血再灌註模型,將實驗動物分假手術組、對照組、治療組。分彆在各箇時間點按照相應程序採集標本檢測肝組織髓過氧化物酶(MPO)活性、免疫組化檢測黏附分子錶達及肝組織誘生型一氧化氮閤酶iNOS mRNA錶達測定。結果肝髒缺血再灌註損傷後,對照組肝髒組織中MPO活性增高,而治療組肝髒組織MPO活性明顯低于對照組(t分彆=3.30、3.10、4.10、2.90,P均<0.05);同時在治療組中炎性趨化因子的錶達也較對照組明顯減低(t分彆=3.70、4.30、4.60、4.90、3.50、4.00,P均<0.05)。免疫組化結果顯示對照組肝組織內可見P-選擇素(P-selectin)及細胞間黏附分子-1(ICAM-1)在肝組織中錶達,而治療組錶達暘性率明顯低于對照組;iNOS的mRNA錶達水平在3 h和6 h時治療組明顯低于對照組(t分彆=4.50、5.70,P均<0.05)。結論 FR167653能在多箇環節、多箇層次對缺血再灌註肝髒起著保護作用。
목적:탐토P38사렬원활화단백격매(p38MAPK)특이성활성억제제(FR167653)대대서간장결혈재관주손상보호작용적궤리。방법이용봉폐군SD대서간장부분결혈재관주모형,장실험동물분가수술조、대조조、치료조。분별재각개시간점안조상응정서채집표본검측간조직수과양화물매(MPO)활성、면역조화검측점부분자표체급간조직유생형일양화담합매iNOS mRNA표체측정。결과간장결혈재관주손상후,대조조간장조직중MPO활성증고,이치료조간장조직MPO활성명현저우대조조(t분별=3.30、3.10、4.10、2.90,P균<0.05);동시재치료조중염성추화인자적표체야교대조조명현감저(t분별=3.70、4.30、4.60、4.90、3.50、4.00,P균<0.05)。면역조화결과현시대조조간조직내가견P-선택소(P-selectin)급세포간점부분자-1(ICAM-1)재간조직중표체,이치료조표체양성솔명현저우대조조;iNOS적mRNA표체수평재3 h화6 h시치료조명현저우대조조(t분별=4.50、5.70,P균<0.05)。결론 FR167653능재다개배절、다개층차대결혈재관주간장기착보호작용。
Objective To research the protection of p38MARK inhibitor FR167653 to the liver ischemia reperfusion in-jury in rats. Methods Liver ischemic reperfusion injury models of SD rats were structured and divided into sham operation group, control group and treatment group. Samples were harvested and used for detecting immunohistochemistry, activity of MPO and iNOS mRNA. Results After liver ischemic reperfusion injury, the activity of MPO in control group increased which was significantly higher than that in treatment group (t=3.30, 3.10,4.10,2.90,P<0.05). Meanwhile, the expression of chemokine in treatment group was significantly lower than control group (t=3.70, 4.30, 4.60,4.90,3.50,4.00,P<0.05). P-selectin and ICAM-1 were expressed dispersedly in the hepatic tissue after ischemic reperfussion injury in control group which were significantly higher than treatment group. In the control group, the expression of iNOS mRNA at 3-hour and 6-hour were significantly higher than treatment group(t=4.50,5.70,P<0.05). Conclusion FR167653 can protect liver from ischemia reperfusion injury.