摘要
目的:观察预电针止痒穴对“曲池”“血海”对荨麻疹(UR)的防治作用,并探讨其调节炎性反应的机制。方法:取3只SD大鼠采用卵蛋白与免疫佐剂联合注射法制备抗卵蛋白血清,再将16只SD大鼠采用皮肤被动过敏反应法制备UR模型,随机分为模型组、预电针组,每组8只,另取8只大鼠作为空白组。预电针组电针“曲池”“血海”预处理,1次/d,连续10 d。造模0.5 h后,记录0.5 h内大鼠搔抓背部致敏皮肤次数,HE染色法观察皮肤组织病理变化,甲苯胺蓝染色法观察皮肤、血液、肠系膜及腹腔液肥大细胞(MCs)形态并计算脱颗粒率,免疫组织化学法检测皮下组织免疫球蛋白E(IgE)、组胺(HIS)、5-羟色胺(5-HT)表达,Western blot法检测皮肤组织中细胞焦亡相关分子NOD样受体热蛋白结构域相关蛋白3(NLRP3)、凋亡相关微粒蛋白(ASC)、半胱氨酸天冬氨酸酶-1(Caspase-1)蛋白表达水平,ELISA法检测血清白细胞介素(IL)-1β、IL-18含量。结果:与空白组比较,模型组大鼠搔抓致敏皮肤次数显著增加(P<0.01),致敏皮肤伊文斯蓝渗出量增多(P<0.01),致敏皮肤组织炎性反应明显,皮肤、血液、肠系膜与腹腔液MCs脱颗粒率显著增加(P<0.01),皮下组织IgE、HIS、5-HT阳性表达及皮肤组织NLRP3、ASC、Caspase-1蛋白表达水平与血清IL-1β、IL-18含量均显著升高(P<0.01,P<0.05)。与模型组比较,预电针组大鼠搔抓致敏皮肤次数显著下降(P<0.01),致敏皮肤伊文斯蓝渗出量降低(P<0.01),致敏皮肤组织炎性反应减轻,皮肤、血液、肠系膜与腹腔液MCs脱颗粒率显著下降(P<0.01),皮下组织IgE、HIS、5-HT阳性表达及皮肤组织NLRP3、ASC、Caspase-1蛋白表达水平与血清IL-1β、IL-18含量均显著下降(P<0.01,P<0.05)。结论:预电针止痒对穴“曲池”“血海”可通过抑制炎性反应防治UR,该效应与针刺调节过敏反应及细胞焦亡两种途径有关。
Objective To observe the effect of electroacupuncture(EA)preconditioning at“Quchi”(LI11)and“Xuehai”(SP10)in prevention of urticaria.Methods Twenty-four male SD rats were randomly divided into control,model and preconditioning of EA(Pre-EA)groups(8 rats/group).The urticaria model was established by intradermal injection of dilute allogeneic antioalbumin serum at the spots of the bilateral symmetry of the spine on the back,and followed by tail venous injection of mixture solution of egg albumin diluent,plus 0.5%Evans blue and normal saline.Ten days before the end of modeling,rats of the pre-EA group received EA stimulation of LI11 and SP10 for 20 min,once a day for 10 consecutive days.The times of rat’s scratching the sensitized skin were recorded.HE staining method was used to observe the pathological changes of skin tissue,and toluidine blue staining method was used to observe the morphology of mast cells(MCs)in the skin,blood,mesentery,and peritoneal fluid,and calculate the degranulation rate.Immunohistochemical stainning was used to detect immunoglobulin E(IgE),histamine(HIS),and 5-hydroxytryptamine(5-HT)expressions in subcutaneous tissue.NOD like receptor thermal domain associated protein 3(NLRP3)inflammasome,apoptosis related granule protein(ASC),and cysteine aspartate aminotransferase 1(Caspase-1)protein expression levels in skin tissue were detected by Western blot.The contents of serum interleukin(IL)-1βand IL-18 were detected using ELISA method.Results Compared with the control group,the scratching times,amount of Evans blue exudation of the sensitized blue spots,degranulation rate of MCs in skin,blood,mesentery and peritoneal fluid,the expression levels of IgE,HIS,5-HT in subcutaneous tissue,protein expression levels of NLRP3,ASC,Caspase-1 in skin tissue,and the contents of serum IL-1βand IL-18 were significantly increased(P<0.01,P<0.05)in the model group.In comparison with the model group,the scratching times,amount of Evans blue exudation of the sensitized blue spots,degranulation rate of MCs,the expression levels of IgE,HIS,5-HT in subcutaneous tissue,protein expression levels of NLRP3,ASC,Caspase-1 in skin tissue,and the contents of serum IL-1βand IL-18 in EA group were significantly decreased(P<0.01,P<0.05).Conclusion EA preconditioning at LI11 and SP10 can prevent and treat UR by inhibiting inflammatory response,which is related to the regulation of pyroptosis.
作者
李记泉
马铁明
李思佳
王巍
金颖
陈怡然
马俊杰
王列
李格格
丁志国
LI Ji-quan;MA Tie-ming;LI Si-jia;WANG Wei;JIN Ying;CHEN Yi-ran;MA Jun-jie;WANG Lie;LI Gege;DING Zhi-guo(College of Acupuncture-Moxibustion and Tuina,Liaoning University of Traditional Chinese Medicine,Shenyang 110847,China;Key Laboratory of Acupuncture and Moxibustion Biology,Liaoning Provincial Department of Education,Shenyang 110847;College of Traditional Chinese Medicine,Liaoning University of Traditional Chinese Medicine,Shenyang 110847)
出处
《针刺研究》
CAS
CSCD
北大核心
2024年第10期1047-1055,共9页
Acupuncture Research
基金
国家自然科学基金青年基金项目(No.82205253)
辽宁省自然科学基金博士启动基金项目(No.2022-BS-199)
中国博士后科学基金项目(No.2021M693850)
辽宁省教育厅基本科研项目(No.JYTQN2023462)。
关键词
预电针
荨麻疹
炎性反应
过敏反应
细胞焦亡
肥大细胞
Electroacupuncture preconditioning
Urticaria
Inflammatory response
Allergic reaction
Cell pyroptosis
Mast cells
