电针对荨麻疹大鼠腹腔肥大细胞中丝裂原活化蛋白激酶及细胞因子表达的影响  

Electroacupuncture improves cutaneous allergic reaction by inhibiting degranulation of intrape-ritoneal mast cells, MAPK signaling and inflammatory factor levels in urticaria rats

作　　者：张小红[1] 李飞飞 齐越[3] 明彩荣[4] 李荧 潘斯腾 刘思佳 马铁明[5] ZHANG Xiao-hong;LI Fei-fei;QI Yue;MING Cai-rong;LI Ying;PAN Si-teng;LIU Si-jia;MA Tie-ming(Graduate School,Liaoning University of Traditional Chinese Medicine,Shenyang 110032,China;State Key Laboratory of Natural and Biomimetic Drugs of Peking University,Beijing 100191;Second Affiliated Hospital,Liaoning University of Traditional Chinese Medicine,Shenyang 110032;Basic Medical Sciences,Liaoning University of Traditional Chinese Medicine,Shenyang 110032;School of Acupuncture-moxibustion and Tuina,Liaoning University of Traditional Chinese Medicine,Shenyang 110032)

机构地区：[1]辽宁中医药大学研究生学院,沈阳110032 [2]北京大学天然药物及仿生药物国家重点实验室,北京100191 [3]辽宁中医药大学附属第二医院,沈阳110032 [4]辽宁中医药大学基础医学院,沈阳110032 [5]辽宁中医药大学针灸推拿学院,沈阳110032

出　　处：《针刺研究》2020年第4期299-304,共6页Acupuncture Research

基　　金：辽宁省教育厅科学技术研究项目(No.L201946);辽宁省创新团队项目(No.LT2015016)。

摘　　要：目的:观察电针对荨麻疹大鼠腹腔肥大细胞脱颗粒及丝裂原活化蛋白激酶(MAPK)和肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6表达的影响,探讨电针干预荨麻疹的生物学机制。方法:SD大鼠随机分为空白组、模型组、电针组、阳性药物组,每组8只。采用皮肤被动过敏反应制备荨麻疹大鼠模型。电针组电针双侧"曲池""血海""足三里",疏密波,频率2 Hz/15 Hz,电流强度1 mA,1次/d,每次20 min,连续7 d;阳性药物组予氯雷他定(1 mg·kg^-1·d^-1)灌胃,连续7 d。观察4组大鼠背部皮肤组织所出现蓝斑的直径;腹腔肥大细胞悬液涂片观察脱颗粒情况;ELISA法检测腹腔TNF-α、IL-6含量;Western blot法检测腹腔肥大细胞MAPK信号通路相关蛋白表达水平。结果:空白组大鼠背部皮肤未出现蓝斑,模型组大鼠背部皮肤出现直径较大的蓝斑,两组蓝斑直径比较差异有统计学意义(P<0.01),电针组、阳性药物组蓝斑直径较模型组明显缩小(P<0.01)。与空白组比较,模型组腹腔肥大细胞脱颗粒率及TNF-α、IL-6含量均明显增加(P<0.01);与模型组比较,电针组、阳性药物组腹腔肥大细胞脱颗粒率及TNF-α、IL-6含量均明显降低(P<0.01,P<0.05)。与空白组比较,模型组肥大细胞p-ERK、ERK、p-JNK、JNK、p-P38MAPK、P38MAPK蛋白表达水平明显增加(P<0.01,P<0.05);与模型组比较,电针组肥大细胞p-ERK、p-JNK、JNK、p-P38MAPK蛋白表达水平明显降低(P<0.05),阳性药物组肥大细胞p-ERK、p-JNK、JNK、p-P38MAPK、P38MAPK蛋白表达水平明显降低(P<0.05);与电针组比较,阳性药物组肥大细胞P38MAPK蛋白表达水平明显降低(P<0.05)。结论:电针可通过抑制荨麻疹大鼠肥大细胞脱颗粒而发挥抗过敏作用,其机制可能与调控肥大细胞MAPK信号通路相关蛋白及TNF-α、IL-6细胞因子的表达有关。Objective To observe the effect of electroacupuncture(EA) on degranulation of intraperitoneal mast cells(MCs) and expression of mitogen-activated protein kinase(MAPK) signaling related proteins, tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) in urticaria rats, so as to reveal its mechanisms underlying improvement of urticaria. Methods Thirty-two SD rats were randomly divided into control,model,EA and medication groups(n=8 in each group). The urticaria model was established by using passive cutaneous anaphylaxis(PCA) reaction method. EA(2 Hz/15 Hz, 1 mA) was applied to bilateral "Zusanli"(ST36), "Quchi "(LI11) and "Xuehai"(SP10) for 20 min,once daily for 7 consecutive days before antigen attack. Rats of the medication group were treated by gavage of Loratadine(1 mg·kg^-1·d^-1)for 7 days. The diameter of cutaneous Evan’s blue spots was measured to evaluate the severity of PCA. Intraperitoneal fluid smears were prepared to observe the degranulation state of MCs. The contents of TNF-α and IL-6 in the intraperitoneal fluid were detected by ELISA, and the expression of extracellular signal-regulated kinase(ERK), phosphorylated(p)-ERK, c-Jun N-terminal kinase(JNK), p-JNK, P38 MAPK and p-P38 MAPK of the acquired intraperitoneal MCs was detected by Western blot. Results The diameter of cutaneous Evan’s blue spot was significantly increased in the model group than that in the control group(P<0.01), and considerably decreased in both EA and medication groups compared with the model group(P<0.01). After modeling,the percentage of degranulated MCs, contents of TNF-α and IL-6, and expression levels of ERK, p-ERK, JNK, p-JNK, P38 MAPK and p-P38 MAPK were remarkably increased in the mo-del group than those in the control group(P<0.01, P<0.05). After the treatment, the percentage of degranulated MCs, contents of TNF-α and IL-6, and expression levels of p-ERK, JNK, p-JNK and p-P38 MAPK were obviously decreased in both EA and medication groups relevant to the model group(P<0.01, P<0.05), while no significant chan

关 键 词：电针 荨麻疹 MAPK信号通路 肥大细胞脱颗粒 

分 类 号：R245.97[医药卫生—针灸推拿学]