期刊
BMC ANESTHESIOLOGY
卷 16, 期 -, 页码 -出版社
BMC
DOI: 10.1186/s12871-016-0215-0
关键词
Nav1.7; Burn injury pain; Lentiviral vector; shRNA; Dorsal root ganglion
资金
- independent innovation project of Zhengzhou University
- Zhengzhou University, Zhengzhou, Henan, China
- National Natural Science Foundation of China, China [81471144, 81200866]
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 degrees 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.
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