Regulation of mild moxibustion on non-neuronal cholinergic system in ulcerative colitis rats

To investigate the effect and mechanism of mild moxibustion on the non-neuronal cholinergic system (NNCS) in rats with ulcerative colitis (UC).

UC rat model was established by administering 4% dextran sulfate sodium. After 7 d, mild moxibustion, α7 nicotinic acetylcholine receptors (α7nAchRs) antagonist (α-bungarotoxin, α-BGT), vesicular acetylcholine transport inhibitor (vesamicol hydrochloride, VH) and organic cation transporters inhibitor (quinine, Qu) treatments were performed once daily for 7 d. Haematoxylin and eosin staining was used for morphological evaluation of colon tissues. Enzyme-linked immunosorbent assay (ELISA) was used to measure the protein expressions of interleukin-1β (IL-1β) and choline acetyltransferase (ChAT) in colon tissue. Reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the mRNA expressions of IL-1β, carnosine acetyltransferase (CarAT), ChAT, and nuclear factor kappa-B p65 subunit (NF-κB p65) in colon tissue. Western blot was used to detect NF-κB p65 protein expression in colon tissue. Immunofluorescence was used to detect the expressions of neuronal acetylcholine (nAch) and non-neuronal acetylcholine (nnAch, released by NNCS) in colon tissue.

Mild moxibustion inhibited colon inflammation and repaired mucosal damage to the colon in UC rats. Meanwhile, mild moxibustion could downregulate the expressions of IL-1β, NF-κB p65 protein and mRNA (P < 0.01), and upregulate the expressions of ChAT protein and CarAT mRNA (P < 0.05, P < 0.01). The α7nAChR antagonist α-BGT can reverse the protective effect of mild moxibustion on the UC and the inhibitory effect on the inflammatory factors. VH cannot affect the effect of mild moxibustion on the expressions of IL-1β and nnAch, while Qu can reverse the effect of mild moxibustion on the expression of IL-1β and nnAch.

Mild moxibustion can inhibite colon inflammation in UC rats, which is closely related to the release of acetylcholine by NNCS and its mediated mechanism of cholinergic anti-inflammation pathway.