环氧合酶-2和磷酸化P38丝裂原活化蛋白激酶在扁平苔藓皮损中的表达

目的：检测环氧合酶-2（COX-2）及其上游调控蛋白磷酸化P38丝裂原活化蛋白激酶（p-P38MAPK）在扁平苔藓皮损中的表达，探讨其在发病中的意义。方法：采用免疫组化技术检测20例扁平苔藓皮损标本中COX-2和p-P38MAPK的表达情况，20例正常皮肤组织作为对照。结果：20例扁平苔藓皮损标本中COX-2和p-P38MAPK的积分光密度值（IOD）分别为（8.46±1.79）×10³和（11.54±2.85）×103，均明显高于对照组(3.14±2.35)×103和(6.26±3.12)×10³，差别具有统计学意义（均P＜0.01），同时COX-2与p-P38MAPK的表达强度呈正相关（r=0.62，P＜0.01）。结论：扁平苔藓皮损中COX-2表达上调，可能与上游P38MAPK的活化有关，可能是引起扁平苔藓发病的环节之一。     

Enhancement of cell migration by corticotropin-releasing hormone through ERK1/2 pathway in murine melanoma cell line, B16F10

Melanoma is a malignant skin cancer that displays a high rate of tumor cell migration and metastasis. This study examined how corticotropin-releasing hormone (CRH) affects the migration of melanoma cells in order to further understand the relationship between stress and tumor cell migration. The migration assay data showed that CRH treatment increased the level of B16F10 cell migration in a dose- and time-dependent manner. To determine whether the extracellular signal-regulated protein kinase 1/2 (ERK1/2) signaling pathway is involved in the upregulation of melanoma migration, cells were pretreated with an inhibitor of ERK1/2 (PD098059). The pretreatment of PD098059 blocked the increase in cell migration. Furthermore, CRH induced the phosphorylation of ERK1/2. The maximum activation of ERK1/2 by CRH was observed at 15 min. Taken together, these results suggest that CRH is an important mediator that regulates the migration of melanoma cells in the skin during stress through the ERK1/2 signaling pathway.