Identification and analgesic activity study of analgesic protein Ⅶ-2 from venom.

J Venom Anim Toxins Incl Trop Dis

Department of Physiology, Institute of Snake Venom, Wannan Medical College, Wuhu, China.

Published: September 2024

AI Article Synopsis

  • The study examines the role of Acid-sensing ion channel 1a (ASIC1a) in various health conditions and explores new regulatory factors for it.
  • Researchers isolated a protein from venom (named NNAV-Ⅶ-2) that can bind to ASIC1a, using methods like cation exchange chromatography and capillary electrophoresis.
  • Findings showed that NNAV-Ⅶ-2 not only has a significant pain-relieving effect but also reduces the expression of ASIC1a in the spinal cord of rats experiencing inflammatory pain.

Article Abstract

Background: Acid-sensing ion channel 1a (ASIC1a) plays a critical role in physiological and pathological processes. To further elucidate the biological functions of ASICs and their relationships with disease occurrence and development, it is advantageous to investigate and develop additional regulatory factors for ASICs.

Methods: In this study, cation exchange chromatography was used to separate seven chromatographic components from venom. Capillary electrophoresis was employed to detect that Ⅶ peak component containing a main protein Ⅶ-2, which could bind to ASIC1a. The analgesic effects of Ⅶ-2 protein were determined using hot plate methods, and ASIC1a expression in spinal cord tissue from rats with inflammatory pain was detected using western blot.

Results: The purified Ⅶ-2 protein named venom-Ⅶ-2 (NNAV-Ⅶ-2) was obtained by Sephadex G-50 gel filtration, which exhibited a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis with a molecular weight of 6.7 kD. Remarkably, the NNAV-Ⅶ-2 protein demonstrated a significant analgesic effect and downregulated ASIC1a expression in the spinal cord tissue of rats with inflammatory pain.

Conclusions: The analgesic mechanism of the NNAV-Ⅶ-2 protein may be associated with its binding to ASIC1a, consequently downregulating ASIC1a expression in neural tissues.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11398835PMC
http://dx.doi.org/10.1590/1678-9199-JVATITD-2023-0099DOI Listing

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