Copyright
©The Author(s) 2019.
World J Gastroenterol. Apr 21, 2019; 25(15): 1865-1878
Published online Apr 21, 2019. doi: 10.3748/wjg.v25.i15.1865
Published online Apr 21, 2019. doi: 10.3748/wjg.v25.i15.1865
Figure 7 UCB inhibited the TLR4/MyD88/TRAF6/nuclear factor-κB signaling in DSS induced colitis mice.
A: Total protein from colon samples was extracted, and TLR4, MyD88, TRAF6, and IκBα protein expression was measured by western blotting; B-E: Quantification of TLR4, MyD88, TRAF6, and IκBα protein expression was performed by densitometric analysis of the blots. Data are expressed as means ± SEM (n = 3). aP < 0.05 and cP < 0.001 vs control group; dP < 0.05 and fP < 0.001 vs dextran sodium sulfate group. UCB: Unconjugated bilirubin; DSS: Dextran sodium sulfate; TLR4: Toll-like receptor 4; MyD88: Myeloid differentiation primary response gene 88; TRAF6: Tumor necrosis factor receptor-associated factor 6; IκBα: Anti-inhibitor of nuclear factor-κB alpha.
- Citation: Zheng JD, He Y, Yu HY, Liu YL, Ge YX, Li XT, Li X, Wang Y, Guo MR, Qu YL, Qin XF, Jiang MS, Wang XH. Unconjugated bilirubin alleviates experimental ulcerative colitis by regulating intestinal barrier function and immune inflammation. World J Gastroenterol 2019; 25(15): 1865-1878
- URL: https://www.wjgnet.com/1007-9327/full/v25/i15/1865.htm
- DOI: https://dx.doi.org/10.3748/wjg.v25.i15.1865