shRNA mediated knockdown of Nav1.7 in rat dorsal root ganglion attenuates pain following burn injury.
shRNA mediated knockdown of Nav1.7 in rat dorsal root ganglion attenuates pain following burn injury.
复制标题
shRNA 介导的大鼠背根神经节 Nav1.7 敲除可减轻烧伤后的疼痛
DOI：
10.1186/s12871-016-0215-0
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发表时间：
2016-08-11
影响因子：
2.2
通讯作者：
Zang W
中科院分区：
文献类型：
--
作者：
Cai W;Cao J;Ren X;Qiao L;Chen X;Li M;Zang W
Background:Abnormal acute pain after burn injury still torments patients severely. In this study, we investigated that one voltage gated sodium channel Nav1.7 plays a vital role in lowering heat pain threshold after burn injury, and the hypothesis that knockdown of Nav1.7 attenuates pain following burn injury.Methods:Sixty eight adult male Sprague-Dawley rats were divided into 4 treatment groups: (1) sham, which hind paw was put on the room temperature metal plate for 15 s (2) burn model, which hind paw was put on the 85 °C metal plate for 15 s. (3) Burn injury + lentiviral vector -SCN9AsiRNA-GFP (LV- SCN9AsiRNA-GFP group, n = 18), which receive the DRG microinjection of LV- SCN9AsiRNA-GFP on the zero day. (4) Burn injury + lentiviral vector negative control (LV-NC-GFP group, n = 18), which receive the DRG microinjection of empty lentiviral vector on the zero day.Results:Both mechanical and heat threshold were measured from day 1 to 21. Meanwhile, expression of sodium channels Nav1.7 in injured dorsal root ganglia were measured on post-operative days 7(POD 7). Rats exhibited decreased thresholds on both mechanical allodynia and thermal withdrawl latency, accompanied by increased Nav1.7 and c-fos expression in dorsal root ganglion (DRG). And knockdown of Nav1.7 in L5DRG led to the attenuation of burn injury-induced mechanical allodynia and thermal hyperalgesia in the rats.Conclusion:We provide evidence that shRNA mediated knockdown of Nav1.7 attenuates burn induced pain in rats as well as decreased the activiation of c-fos protein.
