Objective To observe the effect of electroacupuncture(EA) of “Shangjuxu”(ST37) and “Tianshu”(ST25) on colonic mucosal injury and activities of nuclear factor-κB(NF-κB)/Nod-like receptor family

pyrin domain-containing 3(NLRP3) inflammasome signaling in the colonic tissue in rats with ulcerative colitis(UC)

so as to explore its mechanisms underlying improvement of UC. Methods Male SD rats were randomly divided into blank

model

medication and EA groups

with 12 rats in each group. The UC model was established by enema of 2-4-6 trinitrobenzene sulfonic acid +50% ethanol(2.5 mL). EA(10 Hz/50 Hz) was applied to bilateral ST37 and ST25 for 20 min

once a day

for a total of 10 days. Rats of the medication group received gavage of mesalazine suspension(2 mL:0.2 g/kg+0.9% saline) once a day

for 10 days. The rats' general conditions were recorded for calculating the disease activity index(DAI) score(0—4 points). The colonic tissue was sampled for giving colonic mucosa damage index(CMDI

0—5 points) score and for observing histopathological changes after hematoxylin-eosin(HE) staining

and for detecting expression levels of NF-κB and NLRP3 by using immunohistochemistry and Western blot

separately. The contents of serum interleukin-1β(IL-1β)

NLRP3 and tumor necrosis factor-α(TNF-α) were detected by enzyme-linked immunosorbent assay. Results Compared with the blank group

the DAI and CMDI scores

contents of serum IL-1β

NLRP3

and TNF-α

as well as the immunoactivity and expression of NF-κB and NLRP3 proteins were significantly increased in the model group(P<0.05). Relevant to the model group

modeling-induced increases of DAI and CMDI scores

serum IL-1β

NLRP3 and TNF-α contents

and NF-κB and NLRP3 expression were reversed in both medication and EA groups(P<0.05)

the effect of EA was apparently superior to that of mesalazine in down-regulating CMDI score and serum IL-1β level(P<0.05). No significant diffe-rences were found between the medication and EA groups in down-regulating DAI score

serum TNF-α and NLRP3 contents

and expression of NF-κB and NLRP3 proteins(P>0.05). The rats' general conditions including arch back sloth

anorexia

loss of fur gloss

weight loss

lethargy and loose of stool

and histopathological changes such as necrosis of intestinal mucosa

formation of obvious ulcerative surface

with many neutrophils and pus cells and inflammatory cell infiltration were obvious in the model group

which were relative milder in both medication and EA groups. Conclusion EA can relieve colonic injury in UC rats

which may be related to its functions in down-regulating serum IL-1β

TNF-α and NLRP3 levels by suppressing colonic NF-κB/NLRP3 inflammasome signaling.