Objective To observe the effect of acupoint catgut embedding(CE) on Nod-like receptor protein 3(NLRP3)/Caspase-1 signaling pathway in “deficiency-stasis” syndrome type ulcerative colitis(UC) rats

so as to explore its mechanisms underlying improvement of UC. Methods A total of 58 male SD rats were randomly divided into control group(10 rats) and model group(48 rats). The “deficiency-stasis” type UC model was established by gavage of adenine and folium sennae solution for 4 weeks

followed by clycter of mixture solution of 5% trinitro-benzene-sulfonic acid and 50% ethanol. A total of 44 UC rats were randomized into model

salicylazosulfapyridine(SASP)

non-acupoint CE

and acupoint CE groups(11 rats in each group). The catgut embedment was applied to bilateral “Zusanli”(ST36)

“Shenshu”(BL23)

“Pishu”(BL20)

“Dachangshu”(BL25)

“Geshu”(BL17) and “Tianshu”(ST25)

or non-acupoints(the fat muscles of the buttocks)

separately

once every two weeks

3 times altogether. Rats of the SASP group received gavage of SASP solution

and those of the other groups received gavage of same amount of normal saline

once daily for 42 days. The rat's general conditions and the colon length were recorded

the disease activity index(DAI

0 to 4 points) and colonic mucosal damage index(CMDI

0 to 5 points) were calculated. Histopathological changes of the colonic mucosa tissue were observed after HE staining

and the tissue damage index(TDI

0 to 6 points) was given. The levels of serum NLRP3

interleukin(IL)-1β and IL-18 were measured by ELISA

and the expression levels of NLRP3

Caspase-1

apoptosis-associated speck-like protein(ASC)

IL-1β and IL-18 mRNAs were measured by fluorescence quantitative PCR. The expression levels of NLRP3 and Caspase-1 proteins in the colon tissues were measured by Western blot

and the immunoactivity of colonic ASC was detected by immunohistochemistry. Results Compared with the control group

the rats' body mass and colonic length were significantly decreased(P<0.01)

and DAI score

CMDI score

TDI score

contents of serum NLRP3

IL-1β and IL-18

expression levels of colonic NLRP3

ASC

Caspase-1

IL-1β and IL-18 mRNAs

and NLRP3 and Caspase-1 proteins as well as colonic ASC immunoactivity were significantly up-regulated in the model group(P<0.01). Compared with the model group

both SASP and acupoint CE groups had a significant increase in body mass and colonic length(P<0.01)

and a marked decrease in DAI score

CMDI score

TDI score

contents of serum NLRP3

IL-1β and IL-18

expression levels of NLRP3

ASC

Caspase-1

IL-1β and IL-18 mRNAs and NLRP3 and Caspase-1 proteins and ASC immunoactivity(P<0.01). The above indexes were improved in the acupoint CE group in relevant to those of the non-acupoint CE group(P<0.01). HE staining of colonic mucosal tissue showed obvious ulcerative surface

destroyed recess

disordered arrangement of glands

mucosal edema and congestion

infiltration of a large number of inflammatory cells in the model group

which was obviously milder in both SASP and acupoint CE groups. Conclusion Acupoint embedding can alleviate colonic injury and inhibit inflammatory reaction in rats with “deficiency-stasis” type UC by down-regulating colonic NLRP3/Caspase-1 signaling.