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. 2021 Nov 8;33(Suppl 1):e922–e932. doi: 10.1097/MEG.0000000000002309

Fig. 7.

Fig. 7.

KIF9-AS1 silencing alleviated the colon injury and inflammation in dextran sulfate sodium (DSS)-induced inflammatory bowel disease (IBD) model. (a) Si-KIF9-AS1 elevated the bodyweight in DSS-induced mice. **P < 0.01 vs. DSS + si-NC; (b) disease activity index (DAI) score of mice was declined by silencing of KIF9-AS1. **P < 0.01 vs. DSS + si-NC; (c) KIF9-AS1 silencing increased the colon length of DSS-induced mice. **P < 0.01 vs. sham; (d–f) the concentrations of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1β in colon tissues of DSS-induced mice were downregulated by KIF9-AS1 knockdown. **P < 0.01 vs. DSS + si-NC; (g) KIF9-AS1 silencing inhibited the expression of KIF9-AS1 in colon tissues of DSS-induced mice. **P < 0.01 vs. DSS + si-NC; (h) downregulation of KIF9-AS1 enhanced the expression of miR-148a-3p in colon tissues of DSS-induced mice. **P < 0.01 vs. DSS + si-NC; (I) KIF9-AS1 knockdown reduced the protein expression of suppressor of cytokine signaling (SOCS3) in colon tissues of DSS-induced mice. **P < 0.01 vs. DSS + si-NC.