Fitzsimmons Bethany L, Zattoni Michela, Svensson Camilla I, Steinauer Joanne, Hua Xiao-Ying, Yaksh Tony L
Department of Anesthesiology, University of California-San Diego, California, USA.
Neuroreport. 2010 Mar 10;21(4):313-7. doi: 10.1097/WNR.0b013e32833774bf.
Pharmacological studies indicate that spinal p38 mitogen-activated protein kinase plays a role in the development of hyperalgesia. We investigated whether either the spinal isoform p38alpha or p38beta is involved in peripheral inflammation evoked pain state and increased expression of spinal COX-2. Using intrathecal antisense oligonucleotides, we show that hyperalgesia is prevented by downregulation of p38beta but not p38alpha, whereas increases in spinal COX-2 protein expression at 8 hours are mediated by both p38alpha and beta isoforms. These data suggest that early activation of spinal p38beta isoform may affect acute facilitatory processing, and both p38beta and alpha isoforms mediate temporally delayed upregulation of spinal COX-2.
药理学研究表明，脊髓p38丝裂原活化蛋白激酶在痛觉过敏的发展中起作用。我们研究了脊髓亚型p38α或p38β是否参与外周炎症引起的疼痛状态以及脊髓COX-2表达的增加。使用鞘内注射反义寡核苷酸，我们发现下调p38β可预防痛觉过敏，而下调p38α则不能，而在8小时时脊髓COX-2蛋白表达的增加由p38α和β亚型共同介导。这些数据表明，脊髓p38β亚型的早期激活可能影响急性易化过程，并且p38β和α亚型均介导脊髓COX-2的时间延迟上调。
