中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2014年
1期
59-61
,共3页
陈峰%张韬%熊江%郭伟%潘秀颉%沈晨阳%宋玉祥%贾森皓%刘杰
陳峰%張韜%熊江%郭偉%潘秀頡%瀋晨暘%宋玉祥%賈森皓%劉傑
진봉%장도%웅강%곽위%반수힐%침신양%송옥상%가삼호%류걸
趋化因子类%主动脉瘤,腹%免疫组化%氢
趨化因子類%主動脈瘤,腹%免疫組化%氫
추화인자류%주동맥류,복%면역조화%경
Chemotactic factors%Aortic aneurysm,abdominal%Immunohistochemistry%Hydrogen
目的 探讨氢气抑制大鼠腹主动脉瘤(AAA)进展的机制.方法 雄性SD大鼠24只,数字表法随机分为AAA组和AAA干预组(腹腔内注射氢气饱和生理盐水),建立AAA模型.术后28 d取材,观察两组腹主动脉扩张情况,用H.E.及弹力纤维特殊染色法检测腹主动脉壁内炎症浸润及中膜弹力纤维破坏情况,用免疫组化染色法检测rCklf1、基质金属蛋白酶(MMP2)的蛋白表达,用实时荧光定量聚合酶链式反应(RT-PCR)测定rCklf1、MMP2的基因表达.结果 AAA组和AAA干预组的腹主动脉扩张率分别为(174 ±21)％和(82±23)％(t=7.682,P＜0.01),瘤壁rCklf1 mRNA表达量分别为5.10 ±0.33和1.34±0.29(t=17.288,P＜0.01),MMP2 mRNA表达量分别为10.28 ±0.35和2.40±0.97(t=15.248,P＜0.01).rCklf1、MMP2主要在AAA瘤壁中层严重病变区表达上调.与AAA组相比,AAA干预组rCklf1和MMP2少量弱阳性表达,动脉壁炎症浸润、弹力纤维破坏降解明显减轻.结论 氢气可能通过抑制rCklf1表达,减少炎症细胞募集到腹主动脉受损区,进而降低MMP2表达合成,从而减缓中膜弹力纤维破坏降解,最终抑制AAA进展.
目的 探討氫氣抑製大鼠腹主動脈瘤(AAA)進展的機製.方法 雄性SD大鼠24隻,數字錶法隨機分為AAA組和AAA榦預組(腹腔內註射氫氣飽和生理鹽水),建立AAA模型.術後28 d取材,觀察兩組腹主動脈擴張情況,用H.E.及彈力纖維特殊染色法檢測腹主動脈壁內炎癥浸潤及中膜彈力纖維破壞情況,用免疫組化染色法檢測rCklf1、基質金屬蛋白酶(MMP2)的蛋白錶達,用實時熒光定量聚閤酶鏈式反應(RT-PCR)測定rCklf1、MMP2的基因錶達.結果 AAA組和AAA榦預組的腹主動脈擴張率分彆為(174 ±21)％和(82±23)％(t=7.682,P＜0.01),瘤壁rCklf1 mRNA錶達量分彆為5.10 ±0.33和1.34±0.29(t=17.288,P＜0.01),MMP2 mRNA錶達量分彆為10.28 ±0.35和2.40±0.97(t=15.248,P＜0.01).rCklf1、MMP2主要在AAA瘤壁中層嚴重病變區錶達上調.與AAA組相比,AAA榦預組rCklf1和MMP2少量弱暘性錶達,動脈壁炎癥浸潤、彈力纖維破壞降解明顯減輕.結論 氫氣可能通過抑製rCklf1錶達,減少炎癥細胞募集到腹主動脈受損區,進而降低MMP2錶達閤成,從而減緩中膜彈力纖維破壞降解,最終抑製AAA進展.
목적 탐토경기억제대서복주동맥류(AAA)진전적궤제.방법 웅성SD대서24지,수자표법수궤분위AAA조화AAA간예조(복강내주사경기포화생리염수),건립AAA모형.술후28 d취재,관찰량조복주동맥확장정황,용H.E.급탄력섬유특수염색법검측복주동맥벽내염증침윤급중막탄력섬유파배정황,용면역조화염색법검측rCklf1、기질금속단백매(MMP2)적단백표체,용실시형광정량취합매련식반응(RT-PCR)측정rCklf1、MMP2적기인표체.결과 AAA조화AAA간예조적복주동맥확장솔분별위(174 ±21)％화(82±23)％(t=7.682,P＜0.01),류벽rCklf1 mRNA표체량분별위5.10 ±0.33화1.34±0.29(t=17.288,P＜0.01),MMP2 mRNA표체량분별위10.28 ±0.35화2.40±0.97(t=15.248,P＜0.01).rCklf1、MMP2주요재AAA류벽중층엄중병변구표체상조.여AAA조상비,AAA간예조rCklf1화MMP2소량약양성표체,동맥벽염증침윤、탄력섬유파배강해명현감경.결론 경기가능통과억제rCklf1표체,감소염증세포모집도복주동맥수손구,진이강저MMP2표체합성,종이감완중막탄력섬유파배강해,최종억제AAA진전.
Objective To explore the mechanism of hydrogen on the intervention of abdominal aortic aneurysm (AAA).Methods Healthy male Sprague-Dawley rats were divided into AAA group and AAA intervention group (saturated hydrogen saline administred intraperitoneally once daily).AAA was induced by infiltration of abdominal arota with 0.5 mol/L calcium chloride.Twenty-eight days later,the diameter of the aorta was measured,and the aortic tissue was exercised for histological examination.The protein location and expression of rCklf1 and matrix metalloproteinase 2 (MMP2) in aortic tissue were observed by immunohistochemistry staining.The mRNA expression of rCklf1 and MMP2 underwent real-time PCR.Results Dilatation rate of abdominal aorta of AAA group and AAA intervention group was (174 ±21) ％ and [(82 ± 23) ％,P ＜ 0.01] respectively.The tissue relative mRNA expression of rCklf1 was 5.10±0.33 and 1.34 ±0.29 (P ＜0.01).The relative mRNA expression of MMP2 was 10.28 ±0.35 and 2.40± 0.97 (P ＜ 0.01).The proteins expression of rCklf1 and MMP2 were mainly increased in the damaged elastic fibers of AAA group.Compared with AAA group,the AAA intervention group had less significant positive expression of rCklf1 and MMP2 protein,infiltration of inflammation,destruction and degradation of elastic fibers.Conclusions Hydrogen which may contribute to reduce rCklf1 expression prevents infiltration of inflammation and expression of MMP2 thus decreasing destruction and degradation of elastic fibers,therefore ameliorates development of AAA.
