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目的探讨白藜芦醇(RES)对肠缺血再灌注致肠黏膜损伤大鼠的保护作用及其可能机制。方法成年雄性SD大鼠24只随机分为假手术组、缺血再灌注损伤组、RES治疗组。假手术组仅分离肠系膜上动脉(SMA)而根部不夹闭。肠缺血再灌注损伤组和RES治疗组均用无损伤血管夹夹闭SMA根部,分别立即经阴茎背静脉注射9 g.L-1盐水、RES(20 mg.kg-1),45 min后放松血管夹形成再灌注。各组大鼠均于制模后6 h采集静脉血和回肠标本。检测血清二胺氧化酶(DAO)及小肠脂肪酸结合蛋白(IF-ABP)水平,应用原位末端转移酶标记法检测肠黏膜上皮细胞凋亡率,HE染色法观察肠组织病理损伤情况。结果肠缺血再灌注6h后,RES治疗组DAO及IFABP水平与肠缺血再灌注损伤组比较显著减少[DAO:(1 650±1 150)U.L-1 vs(2 920±1 520)U.L-1;IFABP:(845.12±123.86)μg.L-1 vs(1 443.76±174.62)μg.L-1,Pa<0.05],但二组较假手术组[(630±150)U.L-1,(26.76±4.86)μg.L-1)]均显著增加(Pa<0.05)。假手术组大鼠肠绒毛顶部、固有层和黏膜下层只有少量散在分布的凋亡细胞,缺血再灌注损伤组大鼠肠黏膜凋亡阳性细胞数量较假手术组明显增加[(66.63±1.71)%vs(9.60±1.76)%,P<0.05],分布范围从绒毛顶部扩大到中、底部,固有层和黏膜下层,细胞凋亡亦明显加重;RES组大鼠肠黏膜细胞凋亡率[(46.72±1.50)%]明显低于缺血再灌注损伤组(P<0.05)。结论 RES对肠缺血再灌注损伤具有保护作用,其机制可能与其抑制肠黏膜上皮细胞凋亡有关。
Objective To investigate the protective effect of resveratrol (RES) on intestinal mucosal damage induced by intestinal ischemia-reperfusion in rats and its possible mechanism. Methods Twenty-four adult male Sprague-Dawley rats were randomly divided into sham operation group, ischemia-reperfusion injury group and RES treatment group. In the sham group, only the superior mesenteric artery (SMA) was isolated and the roots were not clipped. In the ischemia-reperfusion injury group and RES treatment group, the SMA roots were clamped with non-injured vascular clamps. The rats were immediately injected with 9 gL-1 saline and RES (20 mg.kg-1) through the dorsal vein of the penis, and the blood vessels were relaxed after 45 minutes. Clips form reperfusion. All groups of rats collected venous blood and ileal specimens 6 hours after the model preparation. Serum diamine oxidase (DAO) and small intestinal fatty acid-binding protein (IF-ABP) levels were measured. Intestinal epithelial cell apoptosis was detected by in situ terminal transferase labeling. HE staining was used to observe intestinal pathological lesions. Results After 6 hours of intestinal ischemia-reperfusion, the levels of DAO and IFABP in the RES treatment group were significantly decreased compared with the intestinal ischemia-reperfusion injury group [DAO:(1 650±1 150)UL-1 vs(2 920±1 520)UL- 1; IFABP:(845.12±123.86)μg.L-1 vs(1 443.76±174.62)μg.L-1, Pa<0.05], but the two groups were more than sham group [(630±150)UL-1,( 26.76±4.86)μg.L-1)] increased significantly (Pa<0.05). There were only a few scattered apoptotic cells in the apical, lamina propria, and submucosa of intestinal villi in the sham-operated group. The number of apoptosis-positive cells in the intestinal mucosa of the ischemia-reperfusion injury group was significantly higher than that in the sham operation group [(66.63±1.71) %vs(9.60±1.76)%, P<0.05]. Distribution ranged from the top of the villi to the middle and bottom, lamina propria and submucosa. Apoptosis was also aggravated. The rate of apoptosis of the intestinal mucosa in the RES group[( 46.72±1.50)%] was significantly lower than ischemia-reperfusion injury group (P<0.05). Conclusion RES has a protective effect on intestinal ischemia-reperfusion injury, and its mechanism may be related to its inhibition of intestinal epithelial cell apoptosis.