Role of spinal p38alpha and beta MAPK in inflammatory hyperalgesia and spinal COX-2 expression.
Role of spinal p38alpha and beta MAPK in inflammatory hyperalgesia and spinal COX-2 expression.
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DOI：
10.1097/wnr.0b013e32833774bf
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发表时间：
2010-03-10
期刊：
影响因子：
1.7
通讯作者：
Yaksh TL
中科院分区：
文献类型：
--
作者：
Fitzsimmons BL;Zattoni M;Svensson CI;Steinauer J;Hua XY;Yaksh TL
药理学研究表明，脊髓p38 MAPK在痛觉过敏的发展中起作用。我们研究了脊髓亚型p38α或p38β是否参与外周炎症诱发的疼痛状态和脊髓考克斯-2表达的增加。使用鞘内反义寡核苷酸，我们发现痛觉过敏是通过下调p38β而不是p38α来预防的，而脊髓考克斯-2蛋白表达在8小时的增加是由p38α和β亚型介导的。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，p38β和α亚型均介导脊髓考克斯-2的暂时延迟上调。
Pharmacological studies indicate that spinal p38 MAPK plays a role in the development of hyperalgesia. We investigated whether either the spinal isoform p38α or p38β 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 p38β but not p38α, while increases in spinal COX-2 protein expression at eight hours is mediated by both p38α and β isoforms. These data suggest that early activation of spinal p38β isoform may affect acute facilitatory processing, and both p38β and α isforms mediate temporally delayed upregulation of spinal COX-2.