摘要
目的探讨P物质(SP)在变应性接触性皮炎(ACD)小鼠瘙痒中的作用。方法外用2,4-二硝基氟苯(DNFB)建立昆明小鼠ACD模型,观察激发后73h内小鼠的搔抓行为及神经激肽1(NK1)受体拮抗剂spantide和阿片受体拮抗剂纳洛酮对小鼠搔抓行为的影响,并用ELISA、免疫组化分别检测激发后48h小鼠颈背部皮损中SP含量、NK1受体表达。结果ACD小鼠模型在DNFB激发后48h出现搔抓高峰;搔抓高峰时,皮损中SP含量[(3873.40±291.58)pg/g]明显低于阴性对照组[(4349.90±502.83)pg/g](P<0.05),但NK1受体表达(6.13±1.25)明显高于阴性对照组(2.87±0.86)(P<0.05)。Spantide和纳洛酮均可抑制小鼠搔抓行为(P<0.01)。结论DNFB诱发的ACD小鼠模型搔抓行为是瘙痒相关反应;SP通过激活皮肤内NK1受体参与ACD小鼠模型瘙痒的发生。
Objective To investigate the role of substance P （SP） in the pathogenesis of itch in allergic contact dermatitis （ACD） mice. Methods Kunming mice with ACD were established by topical application of 2, 4-dinitrofluorobenzene （DNFB）. The scratching behavior of ACD mice and the effect of spantide （NK1 receptor antagonist） and naloxone （opioid receptor antagonist） were observed at 73h after irritation. SP concentration and NK; receptor expression of skin lesion on the nape were measured by ELISA and immunohistochemistry, respectively at 48h after irritation. Results The scratching bouts of ACD mice peaked at 48h after DNFB irritation. Meanwhile, SP level in the skin lesion of ACD mice was less than that of control group [ （3873. 40±291.58） vs （4349.90±502.83 ） pg/g, P 〈 0.05, whereas NK1 receptor expression in ACD mice was higher than that of control group （6.13±1.25） vs （2.87±0.86） P 〈0.05 ]. Prctreatment with spantide or naloxone significantly suppressed the scratching behavior （ P 〈 0.01）. Conclusions DNFB-indueed scratch in ACD mice is itch-associated response. SP could be implicated in the pathogenesis of itch by activating cutaneous NK1 receptor in ACD mice.
出处
《中国皮肤性病学杂志》
CAS
北大核心
2010年第2期112-114,125,共4页
The Chinese Journal of Dermatovenereology
基金
广东省自然科学基金(7301533)
