中华皮肤科杂志 ›› 2016, Vol. 49 ›› Issue (4): 248-251.

• 论著 • 上一篇    下一篇

磷酸化c-Jun氨基末端激酶和P38丝裂原活化蛋白激酶在寻常性银屑病皮损中的表达

葛新红1,唐真真2,焦亚宁3,吴昊2,喻楠1,董灵娣4,李乐4,杨彪1,蒲小霞2   

  1. 1. 宁夏医科大学总医院皮肤科
    2. 宁夏医科大学
    3. 银川 宁夏医科大学总医院皮肤科
    4. 宁夏医科大学总医院
  • 收稿日期:2015-08-13 修回日期:2016-01-05 出版日期:2016-04-15 发布日期:2016-03-28
  • 通讯作者: 葛新红 E-mail:gexinhong.0101@163.com

Expressions of phosphorylated c-Jun N-terminal kinase and P38 mitogen-activated protein kinase in psoriasis vulgaris lesions

  • Received:2015-08-13 Revised:2016-01-05 Online:2016-04-15 Published:2016-03-28
  • Contact: GE Xin-Hong E-mail:gexinhong.0101@163.com

摘要:

目的 探讨磷酸化c-Jun氨基末端激酶(p-JNK)和P38丝裂原活化蛋白激酶(p-P38MAPK)在寻常性银屑病皮损中的表达。 方法 收集30例确诊的寻常性银屑病患者皮损,同时收集30例健康人皮肤组织作为对照组。采用免疫组化及Western印迹法分别检测p-JNK和p-P38MAPK蛋白在寻常性银屑病皮损组织和正常人皮肤中的表达情况。 结果 免疫组化结果显示,寻常性银屑病皮损组织p-JNK和p-P38MAPK表达的平均吸光度(AOD)值分别为0.663 ± 0.016和0.436 ± 0.011,均明显高于对照组(0.333 ± 0.009和0.306 ± 0.010),差异有统计学意义(t = 44.869、21.913,均P < 0.001)。Western印迹法同样显示,寻常性银屑病皮损p-JNK和p-P38MAPK蛋白相对表达量均显著高于对照组,差异均有统计学意义(t值分别为20.477和165.084,均P < 0.05)。结论 JNK和P38MAPK的活化可能参与了寻常性银屑病表皮细胞的过度增殖。

Abstract:

Ge Xinhong, Tang Zhenzhen, Jiao Yaning, Wu Hao, Yu Nan, Dong Lingdi, Li Le, Yang Biao, Pu Xiaoxia Department of Dermatology, General Hospital of Ningxia Medical University, Yinchuan 750004, China (Ge XH, Jiao YN, Yu N, Dong LD, Li L); Department of Dermatology, Lanling People′s Hospital, Linyi 277700, Shandong, China (Tang ZZ); Ningxia Medical University, Yinchuan 750004, China (Wu H, Yang B, Pu XX) Corresponding author: Ge Xinhong, Email: gexinhong.0101@163.com 【Abstract】 Objective To investigate s of phosphorylated c-Jun N-terminal kinase (p-JNK) and P38 mitogen-activated protein kinase (p-P38MAPK) in psoriasis vulgaris lesions. Methods Tissue specimens were obtained from lesions of 30 patients with psoriasis vulgaris and normal skin of 30 healthy human controls. An immunohistochemical study and Western-blot analysis were performed to measure protein s of p-JNK and p-P38MAPK in these skin specimens. Results As the immunohistochemical study showed, the s of p-JNK and p-P38MAPK (expressed as the average optical density [AOD] value for targeted proteins) were significantly higher in psoriasis vulgaris lesions than in normal skin tissues (p-JNK: 0.663 ± 0.016 vs. 0.333 ± 0.009, t = 44.869, P < 0.001; p-P38MAPK: 0.436 ± 0.011 vs. 0.306 ± 0.010, t = 21.913, P < 0.001). Western-blot analysis also showed increased protein s of p-JNK and p-P38MAPK in psoriasis vulgaris lesions compared with normal skin tissues (t = 20.477, 165.084, respectively, both P < 0.05). Conclusion The activation of JNK and P38MAPK may be involved in the overproliferation of epidermal cells in psoriasis vulgaris lesions.