Niu Huang mitigates dextran sulfate sodium-induced colitis by modulating farnesoid X receptor activation and the complement 3/NLRP3 signaling pathway

Figure 8 Niu Huang attenuates ulcerative colitis by regulating the nuclear factor kappa-B and complement component 3/NOD-like receptor family pyrin domain containing 3 signaling pathways. A and B: Protein expression level of p-P65/P65 in colonic tissues (n = 4 in each group); C: Quantitative polymerase chain reaction analysis of the mRNA expression of Rela (n = 4 in each group); D: Representative images of immunohistochemical of P65 in colon tissues; E: Quantitative analysis of the immunohistochemical results of P65 (n = 3 in each group); F: The upstream transcription factors of complement component 3 were screened using several databases; G: Bindings sites of RELA to complement component 3 were predicted by the JASPAR database; H and I: Protein expression levels of NOD-like receptor family pyrin domain containing 3 and apoptosis-associated speck-like protein containing a CARD in colonic tissues (n = 4 in each group). The original blots are presented in Supplementary Figures 4-6. ^aP < 0.05 vs dextran sulfate sodium group, ^cP < 0.001 vs dextran sulfate sodium group. DSS: Dextran sulfate sodium; NHL: Low-dose Niu Huang group; NHH: High-dose Niu Huang group; Mes: Mesalamine group; C3: Complement component 3; NLRP3: NOD-like receptor family pyrin domain containing 3; ASC: Apoptosis-associated speck-like protein containing a CARD.