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Around 20,000 snakebites are reported annually in Brazil and 90% of them are inflicted by species of the genus Bothrops. Intravenous administration of antibothropic antivenom neutralizes the systemic actions, but it is of little effect on the reversal of local symptoms and often induces adverse reactions, a context that drives the search for complementary treatments for snakebite accidents. Vegetable extracts with a range of antiophidian activities constitute an excellent alternative. In this study, we investigated the anti-hemorrhagic effects of Mouriri pusa Gardn. (Melastomataceae), Byrsonima crassa Niedenzu (Malpighiaceae), Davilla elliptica St. Hill. (Dilleniaceae) and Strychnos pseudoquina St. Hil. (Loganiaceae) against Bothrops jararaca venom. The methanolic extracts from M. pusa (leaves), B. crassa (leaves) and D. elliptica (leaves) showed total neutralization capacity against local hemorrhages. The amenthoflavone and quercetin fractions from B. crassa and the flavonoids fractions (quercetin and myricetin) from M. pusa and D. elliptica also showed total neutralization capacity. We conclude that flavonoids derived from myricetin, quercetin and amenthoflavone play an important role in the anti-hemorrhagic potential of these Brazilian vegetables species against B. jararaca venom.

methanolic extract from Qualea parviflora had gastroprotective effect related to the increase of gastric mucosa defensive factors such PGE(2) levels and maintain the basal gastric glutathione levels. The methanolic extract also showed anti-Helicobacter pylori activity, anti-hemorrhagic effect and antioxidant action, but absence of analgesic, mutagenic and toxic effects, a profile that adds safety to its use.

The phytochemical investigation showed that both extracts possess phenolic acid derivatives, acylglycoflavonoids and condensed tannins with evident quantitative variations that probably influenced the pharmacological differences between extracts.

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The mechanism underlying the role of tumor necrosis factor alpha (TNF‐α) in the development of inflammatory hyperalgesia has been extensively studied, mainly the role of TNF‐α in the release of pro‐inflammatory cytokines. The current concept relies in the fact that TNF‐α stimulates the cascade release of other pro‐inflammatory cytokines, such as IL‐1β, IL‐6, and IL‐8 (CINC‐1 in rats), triggering the release of the final inflammatory mediator prostaglandin E2 (PGE2) and sympathetic amines that directly sensitize the nociceptors. However, this may not be the sole mechanism involved as the blockade of TNF‐α synthesis by thalidomide prevents hyperalgesia without interrupting the synthesis of IL‐1β, IL‐6, and CINC‐1. Therefore, we hypothesized that activation of TNF‐α receptor type 1 (TNFR1) by TNF‐α increases nociceptors’ susceptibility to the action of PGE2 and dopamine. We have found out that intrathecal administration of oligodeoxynucleotide‐antisense (ODN‐AS) against TNFR1 or thalidomide prevented carrageenan‐induced hyperalgesia. The co‐administration of TNF‐α with a subthreshold dose of PGE2 or dopamine that does not induce hyperalgesia by itself in the hind paw of Wistar rats pretreated with dexamethasone (to prevent the endogenous release of cytokines) induced a robust hyperalgesia that was prevented by intrathecal treatment with ODN‐AS against TNFR1. We consider that the activation of neuronal TNFR1 by TNF‐α decisively increases the susceptibility of the peripheral afferent neuron to the action of final inflammatory mediators – PGE2 and dopamine – that ultimately induce hyperalgesia. This mechanism may also underlie the analgesic action of thalidomide.