| Objective: To investigate the mechanism by which moxibustion at Tianshu (ST25) alleviates 5-fluorouracil (5-FU)-induced intestinal mucositis (IM) through regulation of the PPARα-NF-κB/NLRP3 signaling pathway. Methods: An IM mouse model was established using 5-FU. Eighteen C57BL/6 male mice were randomly divided into four groups: blank control (NC), model (IM), moxibustion-15 min (MO 15 min), and moxibustion-30 min (MO 30 min). Pathological changes in colon tissues were observed via hematoxylin-eosin (HE) staining. mRNA expression levels of inflammation-related genes (PPARα, NF-κB, NLRP3, caspase-1, IL-1β, IL-18) were detected by quantitative real-time PCR (RT-qPCR). Protein expression of PPARα, NF-κB, phosphorylated NF-κB (p-NF-κB), and NLRP3 was analyzed using Western blot and immunohistochemistry. Results: Compared to the NC group, the IM group showed significantly shortened colon length (p<0.05), pathological damage (mucosal injury, inflammatory cell infiltration, and glandular disorder), elevated mRNA levels of NF-κB, NLRP3, IL-1β, IL-18, and caspase-1 (p<0.05), and reduced PPARα mRNA and protein expression (p<0.05). After moxibustion intervention, the MO15 group exhibited more pronounced colon length recovery (p<0.05), alleviated pathological damage, significantly downregulated NLRP3 and p-NF-κB protein levels (p<0.05), and increased PPARα protein expression (p<0.05), while total NF-κB protein remained unchanged. Conclusion: Moxibustion at Tianshu (ST25) may mitigate 5-FU-induced intestinal inflammation by activating PPARα to suppress the NF-κB/NLRP3 inflammasome pathway, potentially through modulating oxidative stress and inflammatory cytokine cascades. |
