Herb-partition Moxibustion Relieve Colonic Inflammation in Ulcerative Colitis of DDS-induced Rats Via Dual Inhibition of NF-κB and STAT3 Activation / 世界科学技术-中医药现代化

ABSTRACT

Objective: To observe the effect of herb-partition moxibustion on colonic inflammation in UC rats, and participate in the regulation of immune regulation via NF-κB pathway and STAT3 phosphorylation. Methods: Rats were randomly divided into normal group, the ulcerative colitis group (UC) group and herb-partition moxibustion group, with 8 rats in each group. The rat model of UC was induced by 4％ DSS. After successful modeling, the rats were treated with moxibustion on bilateral Tianshu acupoints (ST25) . Each acupoint was used with 2 Zhuang moxa, 1 time a day, for 7 times. The effect of the herb-partition moxibustion on UC rats was observed by comparing the histopathological and protein concentrations of serum proinflammatory cytokine. Western Blot was used to detect NF-κB pathway and STAT3 activity in colon tissue. Results: Colonic histopathology in the UC group showed that the mucosal epithelium with ulcer formation and obvious inflammatory response. The herb-partition moxibustion could repair colonic epithelial damage and reduce the inflammatory response of colon tissue in UC rats. Compared with the normal group, the serum IL-1β and IL-6 protein concentrations were significantly increased in the UC group (P ＜ 0.05, P ＜ 0.01), and the STAT3 phosphorylation level and protein expression levels of pIκB-α and NF-κB p65 were significantly increased. The protein expression level of IκB-α was significantly decreased. Compared with the UC group, the serum protein concentrations of IL-1β and IL-6 were significantly lower in the herb-partition moxibustion group (P ＜ 0.05), and protein expression level of NF-κB p65 was decreased in the colon tissue. The phosphorylation level of pIκB-α was decreased, while the protein expression level of IκB-α was increased. Conclusion: Herb-partition moxibustion reduced colonic inflammatory response in UC rats by DSS-induced, the underlying mechanism may related to decrease release of proinflammatory cytokines IL-1β and IL-6 via dual inhibition of NF-κB and STAT3 activation.