CAJ | 학술논문

目的探讨Celecoxib对大鼠术后腹腔粘连形成的预防效果及其机制.方法 80只SD大鼠随机分为5组:接受腹膜擦损术为A组,接受腹膜擦损术+40mg/(kg·d)Celecoxib为B组,接受腹膜擦损术+20mg/(kg·d)Celecoxib为C组,接受腹膜擦损术+透明质酸钠凝胶为H组,仅接受开、关腹操作的假手术为S组.各组随机半数大鼠于术后第8天和15天处死,肉眼评估大鼠一般情况和腹腔粘连程度,免疫组化法检测粘连组织VEGF和CD34.结果 5组大鼠术后粘连程度组间差别具有显著性意义(P<0.01),B组、C组的粘连评分均明显小于H组、A组.VEGF蛋白表达量A组最强,次之分别为H组、C组、B组,S组最弱.CD_(34)表达量A组最强,次之分别为H组、C组、B组,S组最弱.结论术后短期口服Celecoxib可有效预防大鼠术后腹腔粘连形成,效果优于透明质酸钠凝胶.机制可能与抑制COX-2活性后下调VEGF表达,抑制粘连组织新生血管发生有关.
목적 탐토Celecoxib대대서술후복강점련형성적예방효과급기궤제.방법 80지SD대서수궤분위5조:접수복막찰손술위A조,접수복막찰손술+40mg/(kg·d)Celecoxib위B조,접수복막찰손술+20mg/(kg·d)Celecoxib위C조,접수복막찰손술+투명질산납응효위H조,부접수개、관복조작적가수술위S조.각조수궤반수대서우술후제8천화15천처사,육안평고대서일반정황화복강점련정도,면역조화법검측점련조직VEGF화CD34.결과 5조대서술후점련정도조간차별구유현저성의의(P<0.01),B조、C조적점련평분균명현소우H조、A조.VEGF단백표체량A조최강,차지분별위H조、C조、B조,S조최약.CD_(34)표체량A조최강,차지분별위H조、C조、B조,S조최약.결론 술후단기구복Celecoxib가유효예방대서술후복강점련형성,효과우우투명질산납응효.궤제가능여억제COX-2활성후하조VEGF표체,억제점련조직신생혈관발생유관.
Objective To determine the preventive effect of Celecoxib on postoperative adhesion formation and its mechanism. Methods We divided 80 SD rats into 5 groups: Groups A, B, C, H and S. Rats in Groups A, B, C and H received the operation of peritoneum rubbing to promote adhesion formation. Group S underwent sham operation. Rats in Group B were given Celecoxib of 40 mg/(kg·d), those in Group C were also given Celecoxib of 20mg/(kg·d), and those in Group H were given sodium hyaluronate (HA) during the operation. On the 8th and 15th postoperative day, half of the rats were sacrificed, the extent of adhesion formation was assessed and the adhesive peritoneum was subjected to immunohistochemistry with VEGF and CD_(34). Results The extent of postoperative adhesion differed significantly among the five groups (P<0.01). Groups B and C had significantly fewer adhesions than Groups H and A. VEGF was expressed most highly in Group A, followed by Groups H, C and B, and most weakly in Group S. CD34 was expressed most highly in Group A, followed by Groups H, C and B, and most weakly in Group S. Conclusion Celecoxib provides durable inhibition of intra-abdominal adhesions in a murine model compared with HA. The mechanism of preventing intra-abdominal adhesion via inhibiting COX-2 is possibly through down-regulated expression of VEGF and reduced microvascular density.