Objective To observe the effect of electroacupuncture(EA) pretreatment at “Quchi ”(LI11) and “Xuehai ”(SP10) on expression of interleukin(IL)-33

suppression of tumorigenicity 2(ST2) and mast cell degranulation in sensitive area of skin tissue in rats with urticaria

so as to explore its mechanisms underlying prevention of urticaria. Methods A total of 32 male SD rats were randomly divided into blank control

model

EA preconditioning and medication groups

with 8 rats in each group. The urticaria model was established by topical injection of the prepared anti-ovalbumin serum(foreign serum

0.1 mL/spot) along the bilateral sides of the spinal column on the back

followed by injection of mixture solution of ovalbumin

0.5% evans blue and normal saline via the tail vein 48 h later. EA intervention(2 Hz/15 Hz

1 mA) was applied to bilateral LI11 and SP10 for 20 min

once daily for 7 d before modeling.Back sensitization was started from the 5

(th)

day on. Rats of the medication group received gavage of loratadine

and those of the model group received gavage of the same volume of normal saline. The diameter of evans blue spots at the back skin tissue was measured; the histopathological changes of the blue spot tissues were observed by light microscope after H.E. staining. The state of degranulation of mast cells in the subcutaneous loose connective tissue was observed by using toluidine blue staining. Serum IgE and histamine contents were detected by ELISA

and the immunoactivity of IL-33 and ST2 in the skin and subcutaneous tissues of the sensitized spots(evans blue exudation spots) was observed by immunohistochemistry. Results Compared with the blank control group

the diameter of evans blue spot

degranulation rate of mast cells

serum IgE and histamine contents

and the immunoactivity of IL-33 and ST2 in the evans blue exudation spot tissues were significantly increased in the model group(P

<

0.01). In comparison with the model group

the increase of the above-mentioned indexes was reversed in both EA and medication groups(P

<

0.01

P

<

0.05). No significant differences were found between the EA and medication groups in down-regulating the levels of the 6 indexes. H.E. staining of the blue spot tissues of rats in the model group showed incomplete structure of the epidermal layer of the skin

unclear interface of tissues

incomplete keratinization

chaotic epidermal cells

disorderly arrangement of fibers in the dermis

and infiltration of inflammatory cells and edema

which was relatively milder in the EA and medication groups. Conclusion EA preconditioning can prevent urticaria(reduce size and sensitive reactions) in rats

which may be associated with its functions in lowering the level of IgE through inhibiting IL-33 and ST2.