中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2011年
21期
1502-1505
,共4页
陈鸣艳%吕宾%陈汉卿%张烁
陳鳴豔%呂賓%陳漢卿%張爍
진명염%려빈%진한경%장삭
受体,蛋白酶激活%肥大细胞%小肠%抗炎药,非甾类
受體,蛋白酶激活%肥大細胞%小腸%抗炎藥,非甾類
수체,단백매격활%비대세포%소장%항염약,비치류
Receptor,protease-activated%Mast cells%Intestine,small%Anti-inflammatoryagent,non-steroidal
目的 观察蛋白酶激活受体2(PAR-2)和肥大细胞在双氯芬酸致小肠黏膜损伤大鼠模型小肠组织中的表达、分布及意义.方法 随机数字表法将24只成年雄性SD大鼠随机分为空白对照组和模型组,每组12只,空向对照组按1 ml/250 g蒸馏水灌胃1次,模型组给予7.5 mg·kg-1·d-1双氯芬酸灌胃1次,至第5天行腹腔注射麻醉,取末端回肠,采用甲苯胺蓝染色法测定小肠黏膜中肥大细胞的分布,并对肥大细胞进行计数;采用免疫组织化学、Western印迹、荧光定量PCR分析PAR-2在小肠黏膜组织中的定位、表达和mRNA的变化.结果 模型组小肠黏膜肥大细胞数明显高于空白对照组(10.3±2.2比4.2±1.2,P＜0.05).免疫组织化学结果显示PAR-2表达于黏膜表面上皮、隐窝上皮和固有层炎性细胞,阳性染色位于细胞质.模型组小肠黏膜中PAR-2 mRNA表达高于空白对照组(2.63±0.26比1,P＜0.05),PAR-2蛋白表达高于空白对照组(24.3±2.4比17.5±3.5.P＜0.05).结论 PAR-2、肥大细胞参与了双氯芬酸致大鼠小肠黏膜损伤过程.PAR-2可能由肥大细胞分泌的类胰蛋白酶激活而参与非甾体抗炎药致小肠损伤的发病过程.
目的 觀察蛋白酶激活受體2(PAR-2)和肥大細胞在雙氯芬痠緻小腸黏膜損傷大鼠模型小腸組織中的錶達、分佈及意義.方法 隨機數字錶法將24隻成年雄性SD大鼠隨機分為空白對照組和模型組,每組12隻,空嚮對照組按1 ml/250 g蒸餾水灌胃1次,模型組給予7.5 mg·kg-1·d-1雙氯芬痠灌胃1次,至第5天行腹腔註射痳醉,取末耑迴腸,採用甲苯胺藍染色法測定小腸黏膜中肥大細胞的分佈,併對肥大細胞進行計數;採用免疫組織化學、Western印跡、熒光定量PCR分析PAR-2在小腸黏膜組織中的定位、錶達和mRNA的變化.結果 模型組小腸黏膜肥大細胞數明顯高于空白對照組(10.3±2.2比4.2±1.2,P＜0.05).免疫組織化學結果顯示PAR-2錶達于黏膜錶麵上皮、隱窩上皮和固有層炎性細胞,暘性染色位于細胞質.模型組小腸黏膜中PAR-2 mRNA錶達高于空白對照組(2.63±0.26比1,P＜0.05),PAR-2蛋白錶達高于空白對照組(24.3±2.4比17.5±3.5.P＜0.05).結論 PAR-2、肥大細胞參與瞭雙氯芬痠緻大鼠小腸黏膜損傷過程.PAR-2可能由肥大細胞分泌的類胰蛋白酶激活而參與非甾體抗炎藥緻小腸損傷的髮病過程.
목적 관찰단백매격활수체2(PAR-2)화비대세포재쌍록분산치소장점막손상대서모형소장조직중적표체、분포급의의.방법 수궤수자표법장24지성년웅성SD대서수궤분위공백대조조화모형조,매조12지,공향대조조안1 ml/250 g증류수관위1차,모형조급여7.5 mg·kg-1·d-1쌍록분산관위1차,지제5천행복강주사마취,취말단회장,채용갑분알람염색법측정소장점막중비대세포적분포,병대비대세포진행계수;채용면역조직화학、Western인적、형광정량PCR분석PAR-2재소장점막조직중적정위、표체화mRNA적변화.결과 모형조소장점막비대세포수명현고우공백대조조(10.3±2.2비4.2±1.2,P＜0.05).면역조직화학결과현시PAR-2표체우점막표면상피、은와상피화고유층염성세포,양성염색위우세포질.모형조소장점막중PAR-2 mRNA표체고우공백대조조(2.63±0.26비1,P＜0.05),PAR-2단백표체고우공백대조조(24.3±2.4비17.5±3.5.P＜0.05).결론 PAR-2、비대세포삼여료쌍록분산치대서소장점막손상과정.PAR-2가능유비대세포분비적류이단백매격활이삼여비치체항염약치소장손상적발병과정.
Objective To identify the expression and significance of protease-activated receptor-2 (PAR-2) and mast cell ( MC) in the rat model of small intestinal mucosal damage by a short-term administration of diclofenac. Methods Twenty-four SD-rats were divided into 2 groups ( control group and model group, 12 rats each) by random digit table. The rats in the control group were treated with 1 ml distilled water per 250 g, once a day while those in the model group diclofenac 7. 5 mg/kg per day. Their terminal ileum was harvested at Day 5 after an intraperitoneal injection. Toluidine blue dyeing was employed to determine the distribution of MC and its count in intestinal mucous membrane. Immunohistochemistry,Western blot and real-time PCR (polymerase chain reaction) were employed analyze the location, expression and change of PAR-2 mRNA in intestinal mucous membrane. Results The count of MC was obviously higher in the model group than that in the control group( 10. 3 ±2. 2 vs 4. 2 ± 1. 2, P ＜0.05 ). PAR-2 was expressed on the mucous surface, recesses epidermis and lamina propria inflammatory cells. And positive dyes were located within cytoplasm. As compared with the control group, the expression of PAR-2 mRNA was higher(2. 63 ±0. 26 vs 1, P ＜0. 05)and its protein expression higher in the model group(24. 3 ±2.4 vs 17. 5 ±3. 5, P＜0. 05). Conclusion Both PAR-2 and mast cell are involved in the pathogenesis of small intestinal mucosa injury induced by diclofenac in rats. PAR-2 may be activated by tryptase released from mast cells and participate in the pathogenesis of small intestinal injury as induced by non-steroidal antiinflammatory drugs.
