中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2012年
37期
2597-2600
,共4页
刘德昭%陈中刚%葛缅%甘小亮%黑子清
劉德昭%陳中剛%葛緬%甘小亮%黑子清
류덕소%진중강%갈면%감소량%흑자청
色甘酸钠%肠缺血再灌注损伤%蛋白酶活化受体-2
色甘痠鈉%腸缺血再灌註損傷%蛋白酶活化受體-2
색감산납%장결혈재관주손상%단백매활화수체-2
Cromolyn sodium%Intestinal ischemia-reperfusion%Protease activated receptor-2
目的 探讨再灌注前应用色甘酸钠对大鼠肠缺血再灌注损伤的影响及与肥大细胞(MC)激活、肠组织蛋白酶活化受体-2 (PAR-2)受体表达的关系.方法 32只SD大鼠通过数字随机法分为4组:假手术组(S组)、缺血再灌注组(IIR组)、色甘酸钠组(CS组)、Compound 48/80组(CP组).每组8只.复制大鼠肠缺血再灌注损伤模型,CS、CP组在再灌注前5 min分别经尾静脉给予色甘酸钠25、0.75 mg/kg,S、IIR组分别给予等量的生理盐水.再灌注3h后活杀大鼠取小肠组织.观察各组肠黏膜病理变化;免疫组化观察类胰蛋白酶表达及MC数量;免疫印迹(Western blot)检测肠组织PAR-2表达.结果 S组肠黏膜Chiu's病理评分(0.75 ±0.21)、MC数量(10±3)、类胰蛋白酶表达(125±15)和肠组织PAR-2受体表达(109±10)最少(P<0.05),CP组病理评分(5.12±0.83)、MC数量(36 ±6)、类胰蛋白酶表达(192±18)和肠组织PAR-2受体表达(211±14)均最多(P<0.05);CS组肠黏膜Chiu's病理评分(2.14 ±0.64)、MC数量(15±4)、类胰蛋白酶表达(138±17)和肠组织PAR-2受体表达(124±12)均明显少于IIR组和CP组(P<0.05).结论 色甘酸钠可能通过稳定肥大细胞膜,抑制类胰蛋白酶表达,进而抑制PAR-2信号通路,从而减轻肠缺血再灌注所致肠损伤.
目的 探討再灌註前應用色甘痠鈉對大鼠腸缺血再灌註損傷的影響及與肥大細胞(MC)激活、腸組織蛋白酶活化受體-2 (PAR-2)受體錶達的關繫.方法 32隻SD大鼠通過數字隨機法分為4組:假手術組(S組)、缺血再灌註組(IIR組)、色甘痠鈉組(CS組)、Compound 48/80組(CP組).每組8隻.複製大鼠腸缺血再灌註損傷模型,CS、CP組在再灌註前5 min分彆經尾靜脈給予色甘痠鈉25、0.75 mg/kg,S、IIR組分彆給予等量的生理鹽水.再灌註3h後活殺大鼠取小腸組織.觀察各組腸黏膜病理變化;免疫組化觀察類胰蛋白酶錶達及MC數量;免疫印跡(Western blot)檢測腸組織PAR-2錶達.結果 S組腸黏膜Chiu's病理評分(0.75 ±0.21)、MC數量(10±3)、類胰蛋白酶錶達(125±15)和腸組織PAR-2受體錶達(109±10)最少(P<0.05),CP組病理評分(5.12±0.83)、MC數量(36 ±6)、類胰蛋白酶錶達(192±18)和腸組織PAR-2受體錶達(211±14)均最多(P<0.05);CS組腸黏膜Chiu's病理評分(2.14 ±0.64)、MC數量(15±4)、類胰蛋白酶錶達(138±17)和腸組織PAR-2受體錶達(124±12)均明顯少于IIR組和CP組(P<0.05).結論 色甘痠鈉可能通過穩定肥大細胞膜,抑製類胰蛋白酶錶達,進而抑製PAR-2信號通路,從而減輕腸缺血再灌註所緻腸損傷.
목적 탐토재관주전응용색감산납대대서장결혈재관주손상적영향급여비대세포(MC)격활、장조직단백매활화수체-2 (PAR-2)수체표체적관계.방법 32지SD대서통과수자수궤법분위4조:가수술조(S조)、결혈재관주조(IIR조)、색감산납조(CS조)、Compound 48/80조(CP조).매조8지.복제대서장결혈재관주손상모형,CS、CP조재재관주전5 min분별경미정맥급여색감산납25、0.75 mg/kg,S、IIR조분별급여등량적생리염수.재관주3h후활살대서취소장조직.관찰각조장점막병리변화;면역조화관찰류이단백매표체급MC수량;면역인적(Western blot)검측장조직PAR-2표체.결과 S조장점막Chiu's병리평분(0.75 ±0.21)、MC수량(10±3)、류이단백매표체(125±15)화장조직PAR-2수체표체(109±10)최소(P<0.05),CP조병리평분(5.12±0.83)、MC수량(36 ±6)、류이단백매표체(192±18)화장조직PAR-2수체표체(211±14)균최다(P<0.05);CS조장점막Chiu's병리평분(2.14 ±0.64)、MC수량(15±4)、류이단백매표체(138±17)화장조직PAR-2수체표체(124±12)균명현소우IIR조화CP조(P<0.05).결론 색감산납가능통과은정비대세포막,억제류이단백매표체,진이억제PAR-2신호통로,종이감경장결혈재관주소치장손상.
Objective To explore the effects of cromolyn sodium (CS) on intestinal ischemiareperfusion (IIR) and its relationship with mast cell activation and protease-activated receptor 2 (PAR-2)expression.Methods A total of 32 SD rats were randomly divided into 4 groups:sham-operated (S),intestinal ischemia reperfusion (IIR),CS (a mast cell stabilizer,CS,25 mg/kg) and compound 48/80 (a mast cell degranulator,CP,0.75 mg/kg) (n =8 each).IIR was induced by clamping superior mesenteric artery for 75 min followed by reperfusion for 3 hours.The above agents were intravenously administrated at 5 min pre-reperfusion.Rats were then sacrificed and intestinal issues harvested for histological examinations.The tryptase expression and mast cell count were analyzed by immunohistochemistry.PAR-2 was analyzed by Western blot.Results The Chiu's score (0.75 ± 0.21),mast cell count (10 ± 3),tryptase expression (125 ± 15) and PAR-2 expression (109 ± 10) of group S were the least while those of group CP the most (all P < 0.05).The Chiu's score (2.14 ± 0.64),mast cell count (15 ± 4),tryptase expression (138 ±17) and PAR-2 expression (124 ± 12) of group CS were less than those of groups IIR and CP (all P <0.05).Conclusion Cromolyn sodium may reduce IIR injury by stabilizing mast cell membrane and inhibiting the expressions of tryptase and PAR-2.