Abstract
Objective. This study explored the mechanism of herb-partitioned moxibustion (HM) on dextran sulfate sodium- (DSS-) induced ulcerative colitis (UC) from the miRNA perspective. Methods. Rats were randomly divided into 3 groups [normal control (NC) group, UC model (UC) group, and herb-partitioned moxibustion (UCHM) group]. The UC and UCHM groups were administered 4% DSS for 7 days. The UCHM group received HM at the Tianshu (bilateral, ST25). The effect of HM on UC was observed and the miRNA expression profile in the colon tissues was analyzed. Results. Compared with the UC group, the body weights were significantly higher in the UCHM group on day 14 (P < 0.001); the macroscopic colon injury scores and microscopic histopathology scores in the UCHM group decreased (P < 0.05); and there were 15 differentially expressed miRNAs in the UCHM group. The changes in miR-184 and miR-490-5p expression levels on the UC were reversed by HM intervention. Validation using qRT-PCR showed that two miRNAs expression trend was consistent with the sequencing results. Conclusion. HM at ST25 might regulate miR-184 and miR-490-5p expression, act on the transcription of their target genes to regulate inflammatory signaling pathways, and attenuate inflammation and tissue injury in the colons of rats with DSS-induced UC.
Highlights
Ulcerative colitis (UC) is a group of chronic, nonspecific, intestinal inflammatory diseases with unclear etiology
We observed that the general condition of rats with dextran sulfate sodium- (DSS-)induced UC treated with herb-partitioned moxibustion (HM) gradually improved, and the increase in body weight was fast, with the body weights on day 14 close to the body weights in the normal group
The increase in body weight was slow, with the body weights on day 14 significantly different from the body weights in the normal control (NC) and UCHM groups
Summary
Ulcerative colitis (UC) is a group of chronic, nonspecific, intestinal inflammatory diseases with unclear etiology. 3.7–5.7% of UC patients have colorectal cancer due to long-term and extensive colonic ulcers and inflammation [3]. The pathogenic factors underlying UC are complicated; genetic and environmental factors have received increasing attention. The pathogenic mechanism is not completely clear, which makes treatment difficult. UC has a long disease course and is prone to recurrence; currently, there is no effective radical measure, and long-term drug treatment is required. The long-term safety of biological products requires confirmation in future studies, and the expensive prices and potential side effects limit their clinical application to some extent [4]. In-depth studies on the pathogenic mechanism of UC are active for both diagnosis and treatment
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