To study the relationship between the cutaneous starting mechanism and the analgesia effect of warm moxibustion on visceral pain by the cutaneous neuronal transient receptor potential vanilloid 1 (nTRPV1). Methods:SPF wild type C57BL/6 mouse were involved in this study. At the week 8, the visceral pain was modeled by 130 μg/mL TNBS injected into the colon in SPF C57BL/6 wild type mice. During the week 12, mice in the Mox group and Sham Mox group received warm moxibustion on ST-36. The cutaneous temperature was controlled around (45±1)℃ in the Mox group while (37±1)℃ in the Sham Mox group. The analgesia effect of moxibustion was assessed by Abdominal withdrawal reflex (AWR). And nTRPV1 in the cutaneous were observed by immunofluorescence which was marked with protein gene product 9.5 (PGP9.5) and TRPV1. Low and high volume capsazepine (CPZ) inhibiting cutaneous TRPV1 activity were involved to observe the changes of analgesia effect and the nTRPV1 expression. Furthermore, sciatic nerve ligation (SNL) and resiniferatoxin (RTX) inhibiting nTRPV1 activity were used to study the differences of analgesia and nTRPV1 expression respectively. Results:Comparing with Sham Mox, Mox significantly reduced the AWR score in the visceral pain mice (P<0.05), and increased the expressions of nTRPV1. After CPZ being involved, the analgesia effect of Mox was inhibited, but low volume CPZ was not able to inhibit the promotion of nTRPV1 by moxibustion. Both SNI and RTX involved were able to inhibit the analgesia and the nTRPV1 of moxibustion. Conclusion:Warm moxibustion is able to improve the pain level of visceral pain which may be mediated by the cutaneous nTRPV1. After blocked the TRPV1 in the skin, the analgesia of warm moxibustion disappeared.