Mechanism of lncRNA-H19 in Intestinal Injury of Mice with Ulcerative Colitis.

INTRODUCTION

Ulcerative colitis (UC) is a debilitating condition of the gastrointestinal system, and long non-coding RNA (lncRNA)-H19 emerges as a crucial player in inflammatory diseases. This study is designed to evaluate the mechanism of H19 in intestinal injury of UC mice and hint at a novel target for UC treatment.

METHODS

UC mouse model was established, followed by injection of shH19, antagomir-331-3p, and tumor necrosis factor receptor-associated factor 4 (TRAF4) overexpression vector. H19, miR-331-3p, and TRAF4 expressions were detected via reverse transcription quantitative polymerase chain reaction. Intestinal injury was appraised via disease activity index (DAI), hematoxylin-eosin staining, and histopathological scoring. Interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-10 levels were detected via enzyme-linked immunosorbent assay. Binding relationships of H19 and miR-331-3p and TRAF4 were verified.

RESULTS

H19 was highly expressed in colon tissues. Silencing H19 attenuated intestinal injury of UC mice, manifested by reductions in weight loss, DAI, histopathological scores, IL-1β and TNF-α, and increases in colon length and IL-10. Mechanically, lncRNA-H19 is bound to miR-331-3p to inhibit its expression. TRAF4 is a target of miR-331-3p. Inhibition of miR-331-3p or overexpression of TRAF4 could reverse the alleviating role of lncRNA-H19 in intestinal injury of UC mice.

CONCLUSION

LncRNA-H19 was highly expressed in UC mice and bound to miR-331-3p to promote TRAF4 transcription, thereby aggravating intestinal injury.