Snakebites represent a serious global public health issue. According to the World Health Organization (WHO), approximately 5.4 million snakebite incidents are reported annually, with around 1.8 to 2.7 million envenoming, resulting in 81,410 to 137,880 deaths, as well as several permanent disabilities, which are three times higher in frequency [1]. Ophidism was initially included in the list of Neglected Tropical Diseases (NTDs) by the WHO in 2009, removed in 2013 [2], and later reinserted in 2017 due to the shortage of antivenoms and pressure from experts and international organizations [3].

In Brazil, Bothrops envenoming is the most frequent, with Bothrops jararacussu being one of the most dangerous species due to the high toxicity of its venom [4]. The abundance of these snakes in rural and forested areas contributes to the high incidence of envenoming, particularly in the Northern and Central-Western regions of the country [5,6]. The venom of B. jararacussu is known to induce severe local and systemic damage, particularly hemorrhage, inflammation, and muscle necrosis [[7], [8], [9]].

Snake venom metalloproteinases (SVMPs) are key components in the pathogenesis of these damages, accounting for approximately 26.2 % of the venom of B. jararacussu. Particularly, BjussuMP-II, a PI class SVMP, is responsible for degrading extracellular matrix components, compromising vascular integrity, and inducing hemorrhage and myonecrosis. Although the standard antivenom treatment is effective in neutralizing the systemic effects of venom, its ability to prevent local tissue destruction is limited, justifying the need for complementary therapeutic approaches [10,11].

Various strategies have been explored to minimize the effects of SVMPs, including monoclonal antibodies [12] and small molecule inhibitors, such as Prinomastat, a metalloproteinase inhibitor [13]. However, these approaches still present significant limitations, such as challenges in bioavailability and high costs [14,15]. Therefore, the search for innovative alternatives to minimize the local damage caused by snake venom is essential.

Photobiomodulation has emerged as a promising strategy for mitigating the toxic effects of venom, with benefits observed in both in vitro and in vivo studies. In vitro, it has been shown to reduce cytotoxicity and reactive oxygen species release, enhance macrophage phagocytic capacity and cell viability, and improve antioxidant enzyme activity [[16], [17], [18], [19], [20], [21]]. In vivo, studies have reported reductions in myotoxicity, hemorrhagic processes, pain, edema, inflammation, and biomarker levels—including alkaline phosphatase, aspartate transaminase, and myoglobin—along with an increase in myogenin transcription [[22], [23], [24], [25], [26], [27], [28], [29], [30]].

The present study aims to investigate the effects of photobiomodulation on myotoxicity and hemorrhage induced by BjussuMP-II, comparing its efficacy with that of conventional antivenom. This study is groundbreaking in evaluating photobiomodulation as a therapeutic approach for intoxication caused by isolated snake venom SVMP.