Role of spinal kindlin-1 in neuropathic pain in rats: the relationship with Wnt3a
10.3760/cma.j.issn.0254-1416.2018.05.019
- VernacularTitle:脊髓kindlin-1在大鼠神经病理性痛中的作用:与Wnt3a的关系
- Author:
Baisong ZHAO
1
;
Yongying PAN
;
Xingrong SONG
Author Information
1. 510623,广州市妇女儿童医疗中心麻醉科
- Keywords:
Connexins;
Wnt proteins;
Neuralgia;
Spinal cord
- From:
Chinese Journal of Anesthesiology
2018;38(5):579-582
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the role of spinal kindlin-1 in neuropathic pain in rats and the relationship with Wnt3a.Methods Eighteen clean-grade healthy male Sprague-Dawley rats,weighing 250-280 g,aged 10-12 weeks,were divided into 3 groups (n =6 each) using a random number table:sham operation group (group S),neuropathic pain group (group NP) and kindlin-1 inhibitor group (group K).Neuropathic pain was induced by chronic compression of the sciatic nerve.The sciatic nerve was only exposed but not ligated in group S.In group K,shRNA was intrathecally injected at 21 days before operation to inhibit the expression of kindlin-1.Vector virus was intrathecally injected at 21 days before operation in S and NP groups.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before operation and 1,4,7,10 and 13 days after operation.Rats were sacrificed at 13 days after measurement of pain threshold and the spinal cord was removed for determination of the expression of kindlin-1 and Wnt3a (by Western blot) and expression of Wnt3a mRNA (by real-time polymerase chain reaction).Results Compared with group S,the MWT was significantly decreased and the TWL was shortened at 4,7,10 and 13 days,and the expression of Wnt3a protein and mRNA and kindlin-1 was up-regulated in group NP (P＜0.05).Compared with group NP,the MWT was significantly increased and the TWL was prolonged at 4,7,10 and 13 days,and the expression of Wnt3a protein and mRNA and kindlin-1 was down-regulated in group K (P＜0.05).Conclusion Kindlin-1 is involved in the development of neuropathic pain by up-regulating the expression of Wnt3a in rats.
