Injecting Botox near the site of a snakebite reduced limb swelling, eased inflammation, and lessened muscle damage in rabbits, a new study shows. The treatment shifted immune cells toward a healing mode, cutting harmful inflammation while boosting repair signals, researchers report in a paper exploring venom from the Deinagkistrodon acutus snake.
“This research could offer fresh perspectives on BoNT/A as a potential treatment for limb damage caused by D. acutus bites,” the study authors note.
Snakebites remain a major health issue around the world, with an estimated 1.8 to 2.7 million cases each year leading to between 81,000 and 138,000 deaths, according to global health reports. In China, bites from the Deinagkistrodon acutus, also known as the sharp-nosed pit viper, often cause severe harm to limbs, including rapid swelling, intense inflammation, and tissue breakdown that can lead to lasting disability or even death.
The venom acts like a destructive force, triggering waves of inflammation and cell death in the affected area. Current treatments, such as surgery to remove damaged tissue or oxygen therapy, often fall short in stopping the progression. That leaves a gap for new approaches to limit the harm early on.
To test Botox, known scientifically as botulinum neurotoxin A, for this purpose, researchers created a model of snakebite injury in rabbits. They injected venom into the animals’ thigh muscles, mimicking a bite, and followed up with antivenom two hours later, as might happen in a clinical setting. In one group, they added Botox injections around the bite site right after the venom exposure.
The results showed clear benefits. Compared to rabbits that received only antivenom, those treated with Botox had less swelling in the limb and lower levels of muscle damage markers in their blood, such as creatine kinase and myoglobin. Tissue samples revealed reduced cell death and milder structural harm, with less edema and fewer signs of necrosis.
“BoNT/A alleviates D. acutus-induced limb injury in rabbits potentially through promoting macrophage polarization,” the researchers conclude.
A key part of the improvement came from changes in inflammation. The venom normally ramps up pro-inflammatory signals, like the molecules TNF-alpha and IL-6, which fuel tissue destruction. Botox treatment lowered these while raising levels of IL-10, a signal that calms inflammation and aids recovery.
Focusing on immune cells called macrophages, which play a central role in the body’s response to injury, the team found that Botox influenced their behavior. These cells can take on different forms: some amplify damage by promoting inflammation, while others help heal by reducing it. After the snakebite, harmful inflammatory macrophages dominated, but Botox shifted the balance toward the healing type, marked by increases in certain proteins like CD206 and Arg1.”These findings suggest that by altering macrophage polarization from a pro-inflammatory M1-dominant state to an anti-inflammatory M2-dominant phenotype, BoNT/A mitigates venom-induced inflammatory muscle damage,” the authors explain.
While the study was done in rabbits and observed effects over just 24 hours, it points to Botox as a possible add-on to existing treatments. More work is needed to determine the best dose, timing, and long-term outcomes, as well as to uncover the exact ways Botox guides these immune shifts.
Citations
P. Lan et al. Botulinum neurotoxin A alleviates Deinagkistrodon acutus venom-induced limb injury through promoting macrophage polarization in rabbits. Toxicon. Published online February 1, 2026. DOI: 10.1016/j.toxicon.2025.108936
