Ulcerative colitis (UC) is a serious digestive system disease. Furthermore, the activation of C3a/C3aR axis promoted the expression of caspase-11. And higher levels of caspase-11 could induce the pyroptosis and inflammation of cells. However, some studies suggested that caspase-11 could promote and suppress the inflammation during the development of UC. In addition, whether C3a/C3aR axis could affect the development of UC by modulating the expression of caspase-11 is unclear. We established the UC rat model in this study. Next, the C3aR inhibitor was used to treat these rats at diverse stages of UC. Next, the HE staining was performed to detect the intestinal damage. ELISA was performed to reveal the expression of IL-6 and TNF-α in different stages of UC. Western blotting was used to detect the expression of caspase-11 and C3aR in different stages of UC. Stimulation of C3aR inhibitor in early stage of UC promoted the expression of C3aR and caspase-11 in later stage of UC. Treatment of C3aR inhibitor in later stage of UC inhibited the expression of C3aR and caspase-11 in later stage of UC. Furthermore, application of C3aR inhibitor in early stage of UC aggravates the damage of colon tissue and enhanced the secretion of TNF-α and IL-6 in the later stage of UC. Treatment of C3aR inhibitor in later stage of UC relieved the symptoms of UC and suppressed the production of TNF-α and IL-6 in the later stage of UC. Application of C3aR inhibitor in early stage of UC induced the poor prognosis of UC by upregulating the expression of caspase-11. Treatment of C3aR inhibitor in later stage of UC relieved the symptoms of UC and lead to the favorable prognosis of UC by inhibiting the expression of caspase-11.

溃疡性结肠炎（UC）是一种严重的消化系统疾病。此外，C3a/C3aR 轴的激活促进了 caspase-11 的表达。并且较高水平的caspase-11可诱导细胞焦亡和炎症。然而，一些研究表明，caspase-11 可以促进和抑制 UC 发展过程中的炎症。此外，C3a/C3aR 轴是否可以通过调节 caspase-11 的表达影响 UC 的发展尚不清楚。我们在本研究中建立了 UC 大鼠模型。接下来，C3aR 抑制剂用于治疗处于 UC 不同阶段的这些大鼠。接下来，进行HE染色以检测肠道损伤。ELISA 检测 UC 不同阶段 IL-6 和 TNF-α 的表达情况。Western blotting检测UC不同阶段caspase-11和C3aR的表达。UC早期C3aR抑制剂的刺激促进了UC晚期C3aR和caspase-11的表达。UC晚期C3aR抑制剂治疗可抑制UC晚期C3aR和caspase-11的表达。此外，UC早期应用C3aR抑制剂会加重结肠组织的损伤，增加UC晚期TNF-α和IL-6的分泌。UC后期C3aR抑制剂治疗可缓解UC症状，抑制UC后期TNF-α和IL-6的产生。C3aR抑制剂在UC早期的应用通过上调caspase-11的表达导致UC预后不良。