白藜芦醇对大鼠重症急性胰腺炎肠道屏障的保护作用

The protective effect of resveratrol on intestinal mucosal barrier in rats with severe acute pancreatitis

目的探讨白藜芦醇(resveratrol,RES)对实验性大鼠重症急性胰腺炎(severe acute pancreatitis,SAP)肠道损伤的保护作用。方法72只SD大鼠随机分为3组:假手术(shamoperation,SO)组、SAP模型组、RES治疗组和SAP组经胰胆管逆行注射40g/L牛磺胆酸钠1mL/kg制备模型,RES组于制模后5min将10g/LRES溶液(20mg/kg)通过阴茎背静脉给药,术后分别在3、6、12h取材。免疫组化SAB法观察回肠固有层及其血管ICAM-1和VCAM-1的表达,放射免疫方法检测血清中TNF-α的含量,同时观察肠道组织SOD和MDA的含量。结果ICAM-1和VCAM-1在SO组呈弱表达,而在SAP组中高表达,RES组表达明显减弱(P<0.05)。SAP组回肠组织的MDA水平升高明显(P<0.05);血清中TNF-α水平显著升高(P<0.05);SOD活性明显降低(P<0.05);RES能明显抑制肠组织中MDA和血清中TNF-α水平而增强SOD活性(P<0.05)。结论RES在SAP的发生中具有抗氧化作用,能抑制TNF-α的产生,抑制ICAM-1和VCAM-1的表达,从而发挥肠黏膜屏障的保护作用。

Objective To explore the protective effect of resveratrol （RES） on the intestinal injury in rats with severe acute pancreatitis （SAP）. Methods Totally 72 SD rats were randomly divided into 3 groups： sham-operation （SO） group, SAP group and RES-treated （RES） group. The SAP models were induced by retrograde injection of 4% sodium taurocholate（0.1 mL/100 g） into biliary-pancreatic duct. In RES group, resveratrol （20 mg/kg） was infused immediately intravenously after SAP model was induced. Samples were obtained at 3, 6 and 12 h after the induction of SAP model, respectively. The expression of intercellular adhesion molecular-1 （ICAM-1） and vascular cell adhesion molecular-1 （VCAM-1） were assessed by immunohistochemical staining. The serum TNF-α was detected by radioimmunity. The activities of superoxide dismutase （SOD） and malondialdehyde （MDA） in the small intestine were detected. Results Significantly decreased SOD （P〈0.05） and increased MDA （ P 〈0.05） in the intestine were observed after the induction of SAP at 3, 6 and 12 h. The serum TNF-α level increased predominantly when compared with SO group （P〈0.05） ; the expression of ICAM-1 and VCAM-1 in the intestine increased in SAP group. RES could inhibit MDA in intestinal tissues and TNF a level in serum, thus enhancing SOD activity. Conclusion RES can produce antioxidative effects, suppress the production of TNF-α as well as the expression of ICAM-1 and VCAM-1 in the intestine, thus protecting intestine mucosal barrier.