L-谷氨酰胺通过p38 MAPK/cPLA2信号通路抑制变应性接触性皮炎

Inhibition of allergic contact dermatitis by L-glutamine through p38 MAPK/cPLA2 signaling pathway

[目的]探讨L-谷氨酰胺(Gln)对变应性接触性皮炎(ACD)模型小鼠的影响及其机制.[方法]利用2,4-二硝基氟苯反复刺激小鼠皮肤建立ACD模型,观察Gln对ACD模型小鼠耳肿胀度、组织病理改变、耳组织p38丝裂原活化蛋白激酶(MAPK)及胞浆型磷酯酶A2(cPLA2)蛋白表达和血清肿瘤坏死因子-α(TNF-α)及白细胞介素4(IL-4)等细胞因子表达的影响.[结果 ]与正常对照组比较,Gln显著抑制ACD模型小鼠耳肿胀度(P<0.05),明显降低皮肤组织p38 MAPK,cPLA2蛋白及血清TNF-α,IL-4炎性细胞因子表达水平(P<0.05).[结论]Gln治疗小鼠ACD有效,机制认为与p38 MAPK/cPLA2信号通路及TNF-α,IL-4炎性细胞因子表达有关系.

OBJECTIVETo explore the effects of L-glutamine on mouse allergic contact dermatitis（ACD）and its mechanisms.METHODS The murine mode1 of ACD induced by 2,4-dinitrofluorobenzene（DNFB）was established.Ear swelling,histopathological changes and the protein expressions of p38 MAPK and cPLA2 in ear tissue were observed,the levels of tumor necrosis factorα（TNF-α）and IL-4 in serum were also determined.RESULTS As compared to the normal control group,L-glutamine could significantly inhibit mouse ear swelling（P〈0.05）,and down-regulate the expressions of p38 MAPK and cPLA2 in skin tissue and the serum levels of TNF-αand IL-4（P〈0.05）.CONCLUSION L-glutamine had therapeutic effects on mouse ACD,the mechanisms maybe associated with p38 MAPK/cPLA2 signaling pathway and the expressions of TNF-αand IL-4.