Copyright
©The Author(s) 2023.
World J Gastroenterol. Jan 21, 2024; 30(3): 252-267
Published online Jan 21, 2024. doi: 10.3748/wjg.v30.i3.252
Published online Jan 21, 2024. doi: 10.3748/wjg.v30.i3.252
Figure 5 NLRP3 overexpression reverses the suppressive effect of SLC6A14 knockdown on lipopolysaccharide-induced FHC cell pyroptosis.
A: CCK-8 assays were performed to determine whether NLRP3 overexpression counteracted the inhibitory effect of SLC6A14 knockdown on lipopolysaccharide (LPS)-induced intestinal epithelial cell (IEC) proliferation; B and C: EdU staining was performed to assess whether NLRP3 overexpression could reverse SLC6A14-mediated promotion of proliferation in LPS-stimulated epithelial cell models; D: Flow cytometry was used to investigate whether NLRP3 overexpression could reverse the proapoptotic effects of SLC6A14 silencing on LPS-treated IECs; E: Quantification of apoptosis. aP < 0.01 vs controls; bP < 0.01 vs LPS; cP < 0.01 vs LPS+sh-SLC6A14. LPS: Lipopolysaccharide; OE: Overexpression.
- Citation: Gu Q, Xia H, Song YQ, Duan J, Chen Y, Zhang Y, Chen HP, Zhang L. SLC6A14 promotes ulcerative colitis progression by facilitating NLRP3 inflammasome-mediated pyroptosis. World J Gastroenterol 2024; 30(3): 252-267
- URL: https://www.wjgnet.com/1007-9327/full/v30/i3/252.htm
- DOI: https://dx.doi.org/10.3748/wjg.v30.i3.252