Regulation of Moxibustion on the Expression of NF-κBp65 and PPARγ mRNA in Colon of Rats with Ulcerative Colitis / 针灸推拿医学（英文版）

ABSTRACT

Objective: To explore the mechanism of herb-partitioned moxibustion for ulcerative colitis (UC) through observing the colonic mucosal histopathological changes and the expression of nuclear factor kappaB (NF-kB) and peroxisome proliferators-activated receptorγ (PPARγ) mRNA of UC rats. ＜br> Methods: Male SD rats were randomly divided into a normal group and a model group. UC model was established by general immunological plus local irritation method. After model identification, rats in the model group were randomly divided into a model group, a herb-partitioned moxibustion (HPM) group and a Western medicine (Salicylazosulfapyridine, SASP) group. Rats in the HPM group received treatment at bilateral Tianshu (ST 25) and Dachangshu (BL 25), two cones for each point, once a day for 7 d. SASP group rats were gavaged with SASP. The pathological scores were evaluated according to hematoxylin-eosin (HE) staining of colonic tissues. We used light microscopy to observe degree of colonic mucosal damage and the quantitative polymerase chain reaction (QPCR) to detect the expression of NF-κBp65 and PPARγ in colorectal mucosa. ＜br> Results: Compared with the normal group, histopathological scores were significantly higher in the model group (P＜0.05); compared with the model group, the scores were decreased significantly in the HPM group and the SASP group. Compared with the normal group, NF-κBp65 mRNA expression was increased with statistical significance in the model group (P＜0.05); compared with the model group, NF-κBp65 mRNA expressions were decreased significantly in the HPM group and the SASP group. Compared with the normal group, PPARγ mRNA expression was increased significantly in the model group (P＜0.05); compared with the model group, PPARγ mRNA expressions were decreased significantly in the HPM group and the SASP group. ＜br> Conclusion: HPM could improve the mucosa damage of UC rats, which is possibly through down-regulating NF-κBp65 to achieve anti-inflammatory effect. Whether decreasing the PPARγ mRNA is possibly involved in preventing precancerosis will need further study.