In recent years, extensive research has delved into the pathophysiology of local reactions triggered by Bothrops snake venoms. Even though antivenom works well at reducing death and systemic effects, it is still not very effective in treating local reactions because the venom works so quickly, and antivenom cannot fix injuries that have already been triggered. This might be attributed to certain molecules amplifying the venom-induced innate response. While evidence suggests endogenous mediators at the venom site play a role in this envenomation, in Brazil, concurrent use of anti-inflammatories or other drugs associated with the antivenom remains uncommon. The aim of this study was to determine how various inflammatory mediators affected the leukocyte-endothelium interaction (LEI) following a B. jararaca bite. According to our findings, nitric oxide and cyclooxygenase pathway eicosanoids significantly contribute to alteration of LEI induced by B. jararaca venom. Conversely, lipoxygenase-mediated eicosanoids, histamine, or serotonin had minimal participation. Markedly, treatment with dexamethasone alongside antivenom mitigated alterations of LEI induced by the B. jararaca snake venom. The limited efficacy of the antivenom in managing Bothrops venom-induced local reactions emphasizes the critical need for supplementary treatments to enhance therapeutic outcomes.

Small RNAs (sRNA) and microRNAs (miRNAs) are small endogenous noncoding single-stranded RNAs that regulate gene expression in eukaryotes. Experiments in mice and humans have revealed that a typical small RNA can affect the expression of a wide range of genes, implying that small RNAs function as global regulators. Here, we used small RNA deep sequencing to investigate at how jararhagin, a metalloproteinase toxin produced from the venom of Bothrops jararaca, affected mmu-miRs expression in mice 2 h and 24 h after injection. The findings revealed that seven mmu-miRs were substantially differentially expressed (p-value (p (Corr) cut-off 0.05, FC 2) at 2h after jararhagin exposure, and that the majority of them were upregulated when compared to PBS. In contrast to these findings, a comparison of Jar 24h vs PBS 24hrs demonstrated that the majority of identified mmu-miRs were downregulated. Furthermore, the studies demonstrated that mmu-miR can target the expression of several genes involved in the MAPK signaling pathway. The steady antithetical regulation of mmu-miRs may correlates with the expression of genes that trigger apoptosis via MAPK in the early stages, and this effect intensifies with time. The findings expand our understanding of the effects of jararhagin on local tissue lesions at the molecular level.