芪仙安肠方对大鼠溃疡性结肠炎的治疗作用及机制

A study on the therapeutic effect and mechanism of Qixiananchang decoction on ulcerative colitis of rats

目的探讨芪仙安肠方对三硝基苯磺酸(TNBS)诱导溃疡性结肠炎模型大鼠的疗效及作用机制。方法采用TNBS诱导制备溃疡性结肠炎大鼠模型40只,随机分为模型组、阳性对照组及芪仙安肠方低、中、高剂量组,各8只,并选未造模大鼠8只作为正常对照组。各组均灌胃给药,模型组和正常对照组予0.9%氯化钠注射液,阳性对照组予柳氮磺吡啶(SASP)0.50g/kg,芪仙安肠方低、中、高剂量组分别给予相应剂量(5.0、10.0、20.0g/kg)的芪仙安肠方原液,均每日1次。给药时间从造模后第3日开始,连续14日。造模后第18日观察各组大鼠结肠黏膜损伤指数(CMDI)及黏膜病理组织学情况,并检测免疫球蛋白(Ig)A、IgG、补体3(C3)、补体4(C4)、肿瘤坏死因子-α(TNF-α)、白细胞介素-2(IL-2)及白细胞介素-4(IL-4)含量变化。结果芪仙安肠方低、中、高剂量组结肠黏膜病理损伤明显改善,CMDI均降低,C3、C4及IL-4含量明显提高,IgA、IgG、TNF-α、IL-2含量降低,与模型组比较差异均有统计学意义(P<0.01);芪仙安肠方中、高剂量组治疗后CMDI、C3、C4、IL-2、IL-4、TNF-α含量与正常对照组比较差异均无统计学意义(P>0.05),与阳性对照组比较差异有统计学意义(P<0.01)。结论芪仙安肠方对TNBS诱导的大鼠溃疡性结肠炎疗效确切,中、高剂量尤其显著,其作用机制可能与免疫调节和减轻细胞因子损伤有关。

Objective To observe the therapeutic effect and mechanism of Qixiananchang decoction on ulcerative colitis of rats induced by trinitrobenzene sulphoacid （TNBS）. Methods 40 SD rats were induced by TNBS and modeled and divided into 5 groups： model group, positive control group, high - dose, mid - dose, low- dose Qixiananchang decoction groups, with 8 rats in each group. There were also 8 non- modeled SD rats in normal control group. All groups were clystered： positive control group was treated by Salazosulfapyridine （SASP） 0.5 g/kg, high- dose, mid- dose and low dose groups were given Qixiananchang decoction respectively （5.0 g/kg, 10.0 g/kg, 20.0 g/kg） from the 3rd day after modehng for 14 days and recorded the changes of the following values： CMDI, mucous membrane histopathology, IgA, IgG, C3, CA, - a（TNF - a）, IL - 2, IL - 4 after 18 days. Results The therapeutic effects in all Qixlananchang decoction groups were superior to those in model control group （ P 〈 0.01 ）. There was no significant differences between mid/high dose groups and normal control group （ P 〉 0.01 ）, and there was a significant difference between mid/high dose groups and positive control group （ P 〈 0.01）. Conclusion Qixiananchang decoction is effective in treatment on ulcerative colitis of rats induced by trinitrobenzene sulphoacid, especially in mid - dose and high - dose groups. Its mechanism may have a close connection with immunoregulation and alleviation of cytokine damages.