天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2013年
9期
891-893
,共3页
郑红波%周洪莲%武亚丽%周丹
鄭紅波%週洪蓮%武亞麗%週丹
정홍파%주홍련%무아려%주단
主动脉瘤,腹%磷酸化酶激酶%大鼠, Sprague-Dawley%磷酸化Akt%磷酸化ERK
主動脈瘤,腹%燐痠化酶激酶%大鼠, Sprague-Dawley%燐痠化Akt%燐痠化ERK
주동맥류,복%린산화매격매%대서, Sprague-Dawley%린산화Akt%린산화ERK
aortic aneurysm,abdominal%phosphorylase kinase%rats,Sprague-Dawley%phosphorylated Akt%phos-phorylated ERK
目的观察磷酸化Akt(p-Akt)和磷酸化ERK(p-ERK)在大鼠腹主动脉瘤模型中的表达情况,探讨腹主动脉瘤的发病机制。方法构建大鼠腹主动脉瘤模型并测量腹主动脉直径,计算直径扩张度;HE染色观察腹主动脉的病理改变;免疫组织化学技术和Western blot技术检测腹主动脉组织中p-Akt和p-ERK的相对表达量。结果腹主动脉瘤组主动脉扩张度(3.689±0.443)明显高于生理盐水组(1.175±0.159)和正常组(1),差异有统计学意义(P<0.05);HE染色显示,腹主动脉瘤组主动脉结构紊乱并有炎症细胞浸润;免疫组化结果和Western blot结果均显示p-Akt在腹主动脉瘤组中的表达明显高于生理盐水组和正常组(P<0.05);p-ERK表达差异不明显(P>0.05)。在腹主动脉瘤组中,p-Akt表达水平与主动脉扩张度呈正相关,p-ERK表达水平与主动脉扩张度无明显相关性。结论 PI3K/Akt信号通路可能参与腹主动脉瘤的发生与发展。
目的觀察燐痠化Akt(p-Akt)和燐痠化ERK(p-ERK)在大鼠腹主動脈瘤模型中的錶達情況,探討腹主動脈瘤的髮病機製。方法構建大鼠腹主動脈瘤模型併測量腹主動脈直徑,計算直徑擴張度;HE染色觀察腹主動脈的病理改變;免疫組織化學技術和Western blot技術檢測腹主動脈組織中p-Akt和p-ERK的相對錶達量。結果腹主動脈瘤組主動脈擴張度(3.689±0.443)明顯高于生理鹽水組(1.175±0.159)和正常組(1),差異有統計學意義(P<0.05);HE染色顯示,腹主動脈瘤組主動脈結構紊亂併有炎癥細胞浸潤;免疫組化結果和Western blot結果均顯示p-Akt在腹主動脈瘤組中的錶達明顯高于生理鹽水組和正常組(P<0.05);p-ERK錶達差異不明顯(P>0.05)。在腹主動脈瘤組中,p-Akt錶達水平與主動脈擴張度呈正相關,p-ERK錶達水平與主動脈擴張度無明顯相關性。結論 PI3K/Akt信號通路可能參與腹主動脈瘤的髮生與髮展。
목적관찰린산화Akt(p-Akt)화린산화ERK(p-ERK)재대서복주동맥류모형중적표체정황,탐토복주동맥류적발병궤제。방법구건대서복주동맥류모형병측량복주동맥직경,계산직경확장도;HE염색관찰복주동맥적병리개변;면역조직화학기술화Western blot기술검측복주동맥조직중p-Akt화p-ERK적상대표체량。결과복주동맥류조주동맥확장도(3.689±0.443)명현고우생리염수조(1.175±0.159)화정상조(1),차이유통계학의의(P<0.05);HE염색현시,복주동맥류조주동맥결구문란병유염증세포침윤;면역조화결과화Western blot결과균현시p-Akt재복주동맥류조중적표체명현고우생리염수조화정상조(P<0.05);p-ERK표체차이불명현(P>0.05)。재복주동맥류조중,p-Akt표체수평여주동맥확장도정정상관,p-ERK표체수평여주동맥확장도무명현상관성。결론 PI3K/Akt신호통로가능삼여복주동맥류적발생여발전。
Objective To observe the expressions of Akt and ERK phosphorylation in abdominal aortic aneurysm of rat model, and explore the pathogenesis of abdominal aortic aneurysm. Methods The rat model of abdominal aortic aneu-rysm was established. The diameter of abdominal aorta was measured and the extended rate of the aorta was calculated. HE staining was used to observe the change of pathology. Immunohistochemistry and Western blot methods were used to detect the expressions of Akt and ERK phosphorylation in the level of protein. Results The dilation of aorta was significantly high-er in abdominal aortic aneurysm group than that of saline group and normal group (P<0.05). HE staining showed structural disorder and inflammatory cell infiltration in abdominal aortic aneurysm group. The results of immunohistochemistry and Western blot results showed that phosphorylation of Akt expression was significantly higher in abdominal aortic aneurysm group than that of saline group and normal group (P<0.05). There was no significant difference in phosphorylation of ERK expression between three groups (P>0.05). Conclusion PI3K/Akt signaling pathway may be involved in the development of abdominal aortic aneurysm.