Role of calpain in spinal dorsal horn in development of paw inflammatory pain in rats
10.3760/cma.j.issn.0254-1416.2011.10.006
- VernacularTitle:脊髓背角卡配因在大鼠足底炎性痛形成中的作用
- Author:
Jingjie WANG
;
Guangjun CHEN
;
Wen CHEN
;
Jin DU
;
Ailun LUO
;
Yuguang HUANG
- Publication Type:Journal Article
- Keywords:
Calpain;
Dorsal horn cells;
Pain;
Inflammation;
Foot
- From:
Chinese Journal of Anesthesiology
2011;31(10):1185-1188
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of calpain in the spinal dorsal horn in development of paw inflammatory pain in rats.Methods Forty-eight male SD rats,aged 6 weeks,weighing 160-200 g,were randomly divided into three groups:normal control group(group C,n =8),PBS group( n =16),zymosan-induced paw inflammatory pain group (group Z,n =24).Inflammatory pain was induced by injection of zymosan 1.25 mg into the plantar surface of left hindpaw.Group PBS received the equal volume of PBS 100 μl.The mechanical paw withdrawal threshold (MWT),paw withdrawal thermal latency (PWTL) and maximum thickness of the plantar surface of left hindpaw were measured before (T0 ) and at 30 min,1,2,4,8,24 and 48 h(T1-7 ) after zymosan or PBS injection.Eight rats were sacrificed at T4 in group PBS and at T4.6,7 in group Z respectively.The left lumbar segment (L4-6) was removed to determination of spectrin α Ⅱ breakdown products,IκBα,cyclooxygenase-2 (COX-2)expression and NF-κB activity in the spinal dorsal horn by Western blot.Results Compared with group C,MWT and PWTL were significantly decreased,maximum thickness of paw and NF-κB activity in the spinal dorsal horn were significantly increased,spectrin α Ⅱ breakdown products and COX-2 expression in the spinal dorsal horn were upregulated,while IκBα expression was down-regulated in group Z( P ＜ 0.05 or 0.01 ),but no significant change was found in group PBS( P ＞ 0.05).Conclusion The activation of calpain in the spinal dorsal horn is involved in the development of paw inflammatory pain in rats through activating NF-κB and up-regulating the expression of COX-2.
