miR‑223‑3p Promotes Ulcerative Colitis Progression in Rhubarb Decoction‑Induced Rats with the Spleen‑Kidney‑Yang Deficiency

Background: Ulcerative colitis (UC) is a prevalent case which needs more detailed exploration. We attempted to illustrate how miR‑223‑3p acted in the development of UC. Materials and Methods: The level of miR‑223‑3p in serum from UC patients was detected using quantitative reverse‑transcriptase polymerase chain reaction. The in vivo experimental spleen‑kidney‑yang deficiency mice model was established to get a better understanding of the action of miR‑223‑3p in UC development. Hematoxylin and eosin staining was applied to observe the intestinal epithelial barrier function. Western blotting was applied to measure the expression of ZO‑1, Occludin, TGF‑β, and Smad3. Results: Enrichment of miR‑223‑3p was observed in serum from UC patients. miR‑223‑3p antagomir could lower the shortening of colon length, alleviating the intestinal epithelial barrier function damage caused by UC. Under the UC conditions, TNF‑α, IL‑6, and IL‑1β were up‑regulated, whereas with the miR‑223‑3p antagomir, the up‑regulation was less pronounced; ZO‑1 and Occludin protein levels were decreased, whereas the decrease was less obvious in the miR‑223‑3p antagomir group. Additionally, miR‑223‑3p regulated UC development through the TGF‑β/Smad3 pathway. Conclusion: miR‑223‑3p promoted UC development with spleen‑kidney‑yang deficiency through the TGF‑β/Smad3 pathway.