Journal
TOXINS
Volume 6, Issue 8, Pages 2363-2378Publisher
MDPI AG
DOI: 10.3390/toxins6082363
Keywords
mu-TRTX-Hhn1b; Nav1.7; analgesic; inflammatory pain; neuropathic pain
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Funding
- National 973 Project of China [2010CB529800, 2012CB22305]
- National Science Foundation of China [21172067]
- Hi-tech Project of Hunan Provincial Development and Reform Commission [20131199]
- Science and Technology Project of Hunan Province [2013SK2015, 2013SK3039, 2014SK3017]
- Scientific Research Key Fund of Hunan Provincial Education Department [13A032]
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mu-TRTX-Hhn1b (HNTX-IV) is a 35-amino acid peptide isolated from the venom of the spider, Ornithoctonus hainana. It inhibits voltage-gated sodium channel Nav1.7, which has been considered as a therapeutic target for pain. The goal of the present study is to elucidate the analgesic effects of synthetic mu-TRTX-Hhn1b on animal models of pain. The peptide was first synthesized and then successfully refolded/oxidized. The synthetic peptide had the same inhibitory effect on human Nav1.7 current transiently expressed in HEK 293 cells as the native toxin. Furthermore, the analgesic potentials of the synthetic peptide were examined on models of inflammatory pain and neuropathic pain. mu-TRTX-Hhn1b produced an efficient reversal of acute nociceptive pain in the abdominal constriction model, and significantly reduced the pain scores over the 40-min period in the formalin model. The efficiency of mu-TRTX-Hhn1b on both models was equivalent to that of morphine. In the spinal nerve model, the reversal effect of mu-TRTX-Hhn1b on allodynia was longer and higher than mexiletine. These results demonstrated that mu-TRTX-Hhn1b efficiently alleviated acute inflammatory pain and chronic neuropathic pain in animals and provided an attractive template for further clinical analgesic drug design.
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