[The role of estrogen in the formation and development of abdominal aortic aneurysm: experiment with rats].
OBJECTIVE
To investigate the role of estrogen in the formation and development of abdominal aortic aneurysm (AAA).


METHODS
Twenty male Wistar rats were randomly divided into 2 equal groups: experiment group, injected with 17-beta estradiol (E2) intraperitoneally 1 week before the establishment of AAA once a day for 3 weeks (until 2 weeks after the establishment of AAA), and underwent infusion of pancreatic elastase into the infrarenal abdominal aorta through a catheter inserted into the left common iliac artery o as to establish the AAA model, and control group, injected with normal saline intraperitoneally for 3 weeks. Two weeks after the establishment of AAA model, the rats underwent laparotomy, blood samples were collected from vena cava inferior to detect the level of E2 by radioimmunoassay and then the aneurysms were harvested to undergo immunohistochemistry and real-time PCR to detect the protein expression and mRNA expression of matrix metalloproteinase (MMP)-2 and MMP-9.


RESULTS
The plasma E2 level of the experiment group was (28+/-6) pg/ml, significantly higher than that of the control group [(5.86+/-0.24) pg/ml, P<0.01]. The aorta dilatation rate of the experiment group was (103+/-4)%, significantly lower than that of the control group [(172+/-13)%, P<0.01]. The destruction of arterial wall, degradation of elastic fibers, and infiltration of inflammatory cells were all more severe in the control group than in the experiment group. The relative mRNA expression of MMP-2 of the experiment group was 0.07+/-0.04, significantly lower than that of the control group (0.22+/-0.07, P<0.01); and the relative mRNA expression of MMP-9 of the experiment group was 1.4+/-0.7, significantly lower than that of the control group (7.4+/-2.8, P<0.01). The protein expression of MMP-2 of the experiment group was (22+/-3)%, significantly lower than that of the control group [(50+/-12)%, P<0.01], and the protein expression of MMP-9 of the experiment group was (23+/-2)%, significantly lower than that of the control group too [(45+/-10)%, P<0.01].


CONCLUSIONS
Estrogen inhibits the AAA formation and development by reducing the MMP-2 and MMP-9 mRNA and protein expression and the infiltration of inflammatory cells.
Wu
Xiao-fei
XF
Third Department of General Surgery, First Affiliated Hospital, China Medical University, Shenyang 110001, China. wxf2001104@yahoo.com.cn
Zhang
Jian
J
Xin
Shi-jie
SJ
Duan
Zhi-quan
ZQ
Zhang
Gong
G
D000818:Animals; D017544:Aortic Aneurysm, Abdominal / Q000097:blood / Q000201:enzymology / Q000517:prevention & control*; D004195:Disease Models, Animal; D004958:Estradiol / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D004967:Estrogens / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology; D007150:Immunohistochemistry; D007274:Injections, Intraperitoneal; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000096:biosynthesis / Q000235:genetics; D020780:Matrix Metalloproteinase 9 / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011863:Radioimmunoassay; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction
D004967:Estrogens; D012333:RNA, Messenger; D004958:Estradiol; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9