Molecular and cellular mechanisms of neuroprotection by oligopeptides from snake venoms

Abstract

Venom snake-derived peptides have multiple biochemical, pharmacological, and toxicological profiles, allowing for the discovery of new medicinal products and therapeutic applications. This review specifically examines the fundamental elements of neuroprotection offered by different oligopeptides derived from snake venom. It also includes a brief evaluation of short peptides that are being considered as potential therapeutic agents. Proline-rich peptides and tryptophyllin family peptides isolated from the crude venom of Viperidae family snakes, specifically Bothrops atrox, Bothrops jararaca, and Bothrops moojeni, have been shown to have pro-survival properties, the ability to reduce oxidative stress, and the ability to promote cell viability and mitochondrial functions. Three significant mechanisms are related to the neuroprotection mediated by snake venom oligopeptides: (1) Activation of the Larginine metabolite pathway, such as polyamines from ornithine metabolism, which reduces N-methyl-D-aspartate (NMDA)-type glutamate receptor activity; (2) Enhancement of cell viability by activating the nerve growth factorsignaling pathway; and (3) Activation of the Muscarinic acetylcholine receptor subtype M1 (mAChR-M1). These small peptides show promise as neuroprotective agents against a variety of neurodegenerative disorders.