清香散治疗实验性结肠炎的作用机理研究

The Mechanism of Qingxiang San for the Treatment of Experimental Colitis

目的:探讨清香散对实验性结肠炎的作用机理。方法:60只大鼠随机分为乙醇组,模型组,清香散低、中、高剂量 组及柳氮磺胺吡啶(SASP)组,每组10只。采用三硝基苯磺酸(TNBS)法制备大鼠实验性结肠炎模型,观察不同剂量清香散对大鼠 体重变化、结肠组织病理损害程度及髓过氧化物酶(MPO)含量变化,并测定结肠超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化 氮(NO)及一氧化氮合酶(NOs)水平。结果:各组大鼠造模后体重明显下降,但3天后逐渐增加,第3天时除低剂量组外,其他 4组与模型组比较,差异有显著性或非常显著性意义(P<0．05,P<0．01);第7天时所有剂量组与模型组比较,差异均有非常 显著性意义(P<0．01)。MPO活性在第7天时低、中、高剂量组均比模型组低,差异有非常显著性意义(P<0．01)。组织学损害 评分,各组与模型组比较,差异有显著性或非常显著性意义(P<0．05,P<0．01)。对模型大鼠结肠组织SOD、MDA、NO、NOs 的影响,各组与模型组比较,差异有显著性或非常显著性意义(P<0．05,P<0．01),表明清香散可降低肠组织MPO、MDA、 NOs及NO含量,升高SOD值。结论:清香散对TNBS致大鼠实验性结肠炎的作用机理可能与其下调结肠组织MDA、NOs及NO 表达水平,上调SOD表达水平有关。

Objective： To explore the mechanism of Qingxiang San （QXS） for experimental colitis. Methods： 60 cases were allocated to alcohol group, model group （MG）, low dosage of QXS group （LDG）, moderate dosage of QXS group, high dosage of QXS group and salazopyrin group, each group 10 rats, the pathogenic damage of colic tissue, the content of myeloperoxidase （MPO）, the superoxide dismutase （SOD）, malondialdehyde （MDA）, nitric oxide （NO） and nitric oxide synthase （NOS） in the colon were observed. Results： The body weights of various group after modelled were markedly decreased, but increased gradually after 3 days. In the third day, the differences were significant or very significant （P〈0.05, P〈0.01） in other 4 groups except LDG. In the7th day the difference of body weight was significant （ P 〈 0.05） between drug groups and MG, and MPO activity was lower in drug group than in MG （ P 〈 0.05）. The scoring of histological damage was significantly different （ P 〈 0.05, P 〈 0.01 ）, indicating that the pathologic damage was reduced. SOD, MDA, NO and NOS of colic tissue in rat models and drug groups were significantly different （ P 〈 0. 05, P 〈 0.01）. It is indicated that Qxs can decrease the content of MPO, MDA, NOS and NO in intestinal tissue and increase the value of SOD. Conclusion： The mechanism of QXS may be related to the decrease of expression level of MPO, MDA NOS and NO and increase of expression level of SOD in rats with experimental colitis.