Objective To observe the protective effect of electroacupuncture(EA) on the intestinal mucosal barrier and its relationship with the Notch/NF-κB signaling pathway in mice with ulcerative colitis(UC)

so as to explore its mechanism of treating UC. Methods Male C57BL/6J mice were randomized into control

model and EA groups

with 6 mice in each group. The UC model was established by giving the mice with 2% Dextran Sulfate Sodium(DSS) for 7 days. EA(2 Hz/15 Hz

0.2 mA) was applied at bilateral “Zusanli”(ST36) for 30 min

once a day for 7 days. The disease activity indexes [DAI=(body weight index score+stool score+bleeding score)/3; 0—4 points] of mice were calculated. The morphological changes of colonic tissues of mice in each group were observed by HE staining

and serum contents of TNF-α and IL-6 were detected by ELISA. Claudin-1 protein expression in colon tissue was detected by immunofluorescence

while the protein expression levels of Muc-2

Notch-1

MMP-9 in colon tissue were detected by immunohistochemistry. The real-time PCR method was used to detect the expression levels of Notch-1

Hes-1

NF-κB

TLR-4 and AKT mRNA in colon tissues. Results After modeling

the DAI

serum TNF-α and IL-6 contents

Notch-1 and MMP-9 protein expression

the relative expression levels of Notch-1

Hes-1

NF-κB

TLR-4 and AKT mRNA in the colonic tissue were significantly increased(P<0.001

P<0.01) in the model group relevant to the control group. At the same time

Claudin-1 and Muc-2 protein expression were significantly reduced(P<0.01). After the EA intervention

the increased DAI score

TNF-α and IL-6 contents

Notch-1 and MMP-9 protein expression

the relative expressions of Notch-1

Hes-1

NF-κB

TLR-4 and AKT mRNA

and the decreased Claudin-1 and Muc-2 protein expression were all reversed compared with the model group(P<0.05

P<0.01

P<0.001). H.E. staining of the colonic tissue showed damage and infiltration of inflammatory cells in the model group

and those were significantly improved in the EA group. Conclusion EA can promote the recovery of intestinal mucosal barrier function and reduce inflammatory reaction in UC mice

which may be associated with its effects in inhibiting the excessive activation of the Notch/NF-κB signaling pathway.