Name: THAMIRYS MARIA PANDOLFI DA FRAGA DA SILVA

Publication date: 08/03/2022
Advisor:

Namesort descending Role
SILVANA DOS SANTOS MEYRELLES Advisor *

Examining board:

Namesort descending Role
ALESSANDRA SIMAO PADILHA Internal Examiner *
CAMILA ALMENARA CRUZ PEREIRA External Examiner *
SILVANA DOS SANTOS MEYRELLES Advisor *

Summary: Euphorbia tirucalli (Aveloz) is a plant originated in Africa, which gained space in tropical regions. It has been used for several therapeutic purposes, its well known for containing a latex rich in bioactive compounds. The (ANVISA) prohibited its commercialization due to the various accidents that can occur when ingested and when in contact with skin and eyes. However, studies have shown that many compounds present in latex have beneficial actions such as antiproliferative, antimicrobial, antioxidant, anti-inflammatory and antimutagenic activities. Objective: To elucidate the effects of E. tirucalli latex on the cardiovascular system, specifically in the aorta arteries of Wistar rats. Methodology: Two 500 ng doses of Aveloz latex (AV) in aqueous medium were standardized and one was subjected to chemical hydrolysis. Then, the animals were sacrificed and the protocol of concentration-response curves to phenylephrine (FE), Acetylcholine (ACh) and Nitroprusside (NPS) were performed before and after the incubation with latex in the bath. Statistical Analysis: Values indicate mean ± SEM. *P<0.05 in relation to the control group. Results: We observed that AV promotes vasoconstriction, and when submitted to the FE curve, they do not respond efficiently when compared to the control. (Ct Rmáx 141.9±3.06% vs. AV Rmáx 107.9±0.94%). When using an alpha 1 adrenergic receptor blocker (prazosin), almost total abolition of contraction was observed in the control group controle (Rmáx 142.7±4.92%) vs. (Ct+Prazosin 107.7±1.42%). However, in the AV group, no difference was observed before and after the blockade. (AV Rmáx 107.9±0.94% vs. AV+Prazosina Rmáx 108.8±2.46%). Because Prazosin inhibits the activation of the Phospholipase C enzyme and consequently the entire cascade of subsequent reactions, this result shows us that Aveloz vessel contraction is due to another pathway. To elucidate whether the vasoconstriction induced by the Aveloz was due to phorbol ester compound, we incubate the vessels with a hydrolyzed form of the latex and the vessel contraction was markedly decreased (Rmax AVH 1.78±44g). Endothelium-dependent vasodilation was evaluated, and in the presence of latex, a decrease of function was observed when compared to control (AV 51.6±10.45%) vs. (Ct 85.23±1.77 %). When using the nitric synthase enzyme inhibitor, L-nitric oxide, a total abolition of relaxation, and reduced NO bioavailability in the AV group was observed AV (AV 51.69±13.49 vs. AV+L-NAME -11.30±2.43) vs. (CT 85.84±1.86 vs. CT+L-NAME -6.11±4.91). Endothelium-independent vasodilation was not different between groups (CT 100.0±0.00 vs. AV 87.77±8.5). These results characterize the plant latex as potent vasoconstrictor, possibly due to the action of phorbol esters, in addition, incubation with Aveloz caused an impairment in the aorta vasodilation in response to ACh.

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