Trypanosoma evansi is a microscopic unicellular protozoan that belongs to the family Trypanosomatidae. It is considered a widely distributed parasite, being the first pathogenic mammalian trypanosome to be described in the world. As a blood and other extracellular fluids parasite, it infects a vast number of wild and domestic mammals, but rarely humans (Desquesnes et al., 2013). T. evansi is spread by mechanical transmission of contaminated blood through hematophagous insects (e.g., Tabanus sp. and Stomoxys calcitrans), and bats (e.g., Desmodus rotundus), causing an important disease called “Surra” in horses, characterized by anemia, immunosuppression, severe neurological signs, hepatosplenomegaly, edema, oxidative stress, rapid weight loss, progressive weakness and death of untreated animals (Baldissera et al., 2017).

The parasite survives and multiplies in the extracellular fluids of their mammalian hosts, especially the blood. They are thus confronted with both innate and adaptive immune defenses, which leads to an inflammatory response unleashing several pro-inflammatory components, such as cytokines (Desquesnes et al., 2013). Most common inflammatory cascades are related to the cyclooxygenase (COX) enzyme, which induces the production of prostaglandins and leads to peripheral nociceptors sensitization, resulting in an inflammatory-like allodynia and pain behavior. Most analgesic drugs prescribed to treat COX-related inflammatory processes are nonsteroidal anti-inflammatory drugs (NSAIDs), with special focus on the select inhibitors of COX-2, the COX isoform that has its expression mainly induced under inflammatory harmful situations (Hilário et al., 2006; Masocha and Kristensson, 2018).

Once pro-inflammatory cytokines may lead to unbalance in the oxidant and antioxidant components, oxidative stress is frequently described in trypanosomosis (Baldissera et al., 2017). The compounds produced when hosts protective paths exacerbate their capacity during infection are capable of causing damage in several structures, such as lipids, proteins, deoxyribonucleic acid (DNA) and tissue cells (Baldissera et al., 2016). As T. evansi presents the capacity to induce immunosuppression in the host, the inflammation and oxidative stress status persist, resulting in a considerable economic impact on country's livestock and economic market (Desquesnes et al., 2013; Dkhil et al., 2020).

The aim of this work was to evaluate allodynia and pain expression through the Right Hind Paw Allodynia (RHPA) and Visceral Allodynia (VA) tests on infected animals. In addition, a NSAID was used as analgesic treatment to verify its capacity to prevent allodynia and pain expression, if present, during T. evansi infection in mice. In addition, through molecular essays, the Myeloperoxidase (MPO) essay evaluated neutrophil infiltration, and oxidative stress was evaluated by evaluating the enzymatic protective system, such as Catalase (CAT) and Reduced Glutathione (GSH) essays, and lipid peroxidation by Malondialdehyde (MDA) essay.