BackgroundNatural antioxidants can reduce oxidative damage caused by high-intensity resistance training (RT). We investigated the in vitro antioxidant potential of hydroethanolic extract (HEE) from Bowdichia virgilioides on muscular damage and oxidative stress in rats subjected to high-intensity RT.MethodsThirty-two male Wistar rats were divided into four experimental groups: 1) control group (CG), oral administration (P.O.) of vehicle; 2) trained group (TG), vehicle-treated with RT; 3) B. virgilioides untrained group (BVG), treated with B. virgilioides HEE (200 mg/kg P.O.); and 4) trained B. virgilioides group (TBVG), treated with B. virgiliodes HEE (200 mg/kg P.O.). All animals were habituated to the training apparatus for 1 week. CT and TBVG animals were subjected to the training protocol, which consisted of three sets of 10 repetitions with 75% of the load established using the one-repetition maximum, for four weeks. CG and BVG animals were manipulated and fixed to the apparatus three times a week with no load. Treatment with B. virgilioides HEE or vehicle treatment was initiated after 25 days of RT (5 days; one dose per day). At the end of the experiments, plasmatic and gastrocnemius samples from all groups were obtained for the assessment of lipid peroxidation and creatine kinase activity.ResultsCompared to TG rats, TBVG rats showed decreases in plasma and gastrocnemius tissue lipid peroxidation by 55.68% (p <0.0001) and 66.61% (p <0.0012), respectively. Further, compared to TG rats TBVG rats showed decreases in plasma and gastrocnemius tissue oxidative stress by 62.83% (p <0.0005) and 54.97% (p <0.0197), respectively.ConclusionsB. virgilioides HEE treatment reduced markers of oxidative stress caused by high-intensity RT. Further, HEE treatment during training significantly reduced the markers of tissue damage.

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The anti-nociceptive and antioxidant activities of the Anadenantheracolubrina stem bark aqueous extract (AEAC) were investigated. AEAC (30 μg/mL) reduced 94.8% of 2,2-diphenyl-1-picrylhydrazyl radical and prevented 64% (200 μg/mL) of lipid peroxidation caused by 2,2'-azobis(2-methylpropionamidine) dihydrochloride-induced peroxyl radicals. AEAC treatment (200 and 400 mg/kg) significantly (p < 0.001) reduced mice orofacial nociception in the first (61.4% and 62.6%, respectively) and second (48.9% and 61.9%, respectively) phases of the formalin test. Nociception caused by glutamate was significantly (p < 0.001) reduced by up to 79% at 400 mg/kg, while 56-60% of the nociceptive behaviour induced by capsaicin was significantly inhibited by AEAC (100-400 mg/kg). Mice treated with AEAC did not show changes in motor performance in the Rota-rod apparatus. It appears that AEAC is of pharmacological importance in treating pain due to its anti-nociceptive effects, which were shown to be mediated by central and peripheral mechanisms.