五味子甲素对小鼠溃疡性结肠炎的治疗作用

Effects of deoxyschisandrin on ulcerative colitis in mice

目的:考察五味子甲素对小鼠溃疡性结肠炎的治疗作用。方法:以三硝基苯磺酸(TNBS)灌肠制备溃疡性结肠炎(ulcerative colitis,UC)小鼠模型,溃疡性结肠炎小鼠随机分为模型组、阳性对照组及五味子甲素高、中、低剂量组(80、40、20 mg/kg),同时设立正常对照组,每组10只。灌胃给药,正常组、模型组分别给予等体积蒸馏水,阳性对照组给予500 mg/kg柳氮磺吡啶(SASP),连续给药14 d。观察五味子甲素对溃疡性结肠炎小鼠临床症状的影响;酶联免疫吸附法(ELISA)检测溃疡性结肠炎小鼠结肠中肿瘤坏死因子-α(TNF-α)及白介素-6(IL-6)水平;用试剂盒检测结肠中髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)及一氧化氮合成酶(TNOS)的活性和丙二醛(MDA)、一氧化氮(NO)的含量。取结肠后HE染色观察组织形态学变化。结果:五味子甲素可改善三硝基苯磺酸诱导的溃疡性结肠炎小鼠临床症状,延长溃疡性结肠炎小鼠结肠转运时间,可显著降低MPO、TNOS活性,升高SOD活性,并降低MDA、NO、IL-6及TNF-α水平。组织病理学检查可见,给予五味子甲素后,溃疡性结肠炎小鼠病变严重程度减轻,动物结肠组织损伤范围明显减少,炎性细胞浸润程度减轻。结论:五味子甲素对三硝基苯磺酸诱导的小鼠溃疡性结肠炎有治疗作用,作用机制可能与其抑制炎症因子NO、IL-6及TNF-α的产生有关。

Objective： To investigate the therapeutic effect of deoxyschisandrin on experimental ulcerative colitis （UC） and possible mechanism. Methods： Trinitrobenzenesulfonic acid（TNBS） inducing UC mice model was prepared. And then UC mice were randomly divided into model group, positive control group, deoxyschisandrin high, medium, and low dose groups （80, 40, 20mg/kg） , and in addition, a normal group was set up. There were 10 mice in each group respectively. The general condition and symptoms changes were observed. Myeloperoxidase （MPO） , SOD and nitric oxide synthase（TNOS） activities and nitric oxide（NO） and MDA levels in colon tissue were determined by biochemical assay. Tumor necrosis factor（TNF-α） and interleukin-6 （IL-6）levels in colon were determined by enzyme-linked immunosorbent assay （ELISA）. In addition, the histopathological examination was performed. Results： Compared with model group, the clinical symptoms were obviously relieved, the colonic transit time was significantly prolonged, and the SOD activity increased, but MPO, TNOS activities and the levels of MDA, NO, IL-6 and TNF-α obviously decreased in UC mice after administrated with different concentrations of deoxyschisandrin for 14 days. Deoxysehisandrin also showed attenuation effect of pathological colon changes in TNBS inducing UC mice. Coneluslon： Deoxy- schisandrin may play its therapeutic role through inhibiting the generation of inflammation factors such as NO, IL-6 and TNF-α.