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 5th 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.
目的：观察针刺预处理“曲池”“血海”对荨麻疹大鼠致敏区域皮肤组织白细胞介素-33(IL-33)、肿瘤抑制素2(ST2)表达及肥大细胞脱颗粒的影响，探讨针刺预处理“曲池”“血海”治疗荨麻疹的作用机制。方法：SD大鼠随机分为空白组、模型组、针刺组、阳性药物组，每组8只。针刺组针刺双侧“曲池”“血海”；阳性药物组给予氯雷他定(1 mg·kg-1·d-1)灌胃，均每日干预1次，连续干预7 d，并于第5天进行背部致敏造模，第7天进行抗原攻击并取材。测量各组大鼠背部皮肤组织蓝斑的直径；HE染色法观察致敏区域皮肤组织形态学变化；甲苯胺蓝染色观察致敏区域皮下疏松结缔组织中肥大细胞脱颗粒情况；ELISA法检测各组大鼠血清IgE及组胺(HIS)含量；免疫组织化学法检测大鼠致敏区域皮肤组织IL-33、ST2的表达。结果：与空白组比较，模型组大鼠蓝斑直径明显增大(P<0.01)，肥大细胞脱颗粒率明显升高(P<0.01)，血清IgE、HIS含量均显著升高(P<0.01)，皮肤组织IL-33、ST2表达显著升高(P<0.01)。与模型组比较，针刺组和阳性药物组蓝斑直径明显缩小(P<0.01)，肥大细胞脱颗粒率明显降低(P<0.01)，血清IgE与HIS含量均降低(P<0.01，P<0.05)，皮肤组织IL-33、ST2表达降低(P<0.01)。HE染色显示，模型组致敏区域皮肤表皮层结构残缺，组织边界不清，角化不完全，表皮细胞混乱，真皮层纤维排列杂乱，有炎性细胞浸润和水肿发生，针刺组和阳性药物组以上病理变化不同程度减轻。结论：针刺“曲池”“血海”可以通过抑制IL-33、ST2的表达来降低血清IgE含量，从而有效改善荨麻疹大鼠症状，起到治疗荨麻疹的目的。.
Keywords: Acupuncture; Interleukin-33; Mast cell degranulation; Suppression of tumorigenicity 2; Urticaria.