Abstract
BackgroundThe aim of the present work was to evaluate the effect of a hexane crude extract (HCE) of Pterodon emarginatus on the oxidative and nitrosative stress induced in skeletal muscle, liver and brain of acutely exercised rats.MethodsAdult male rats were subjected to acute exercise by standardized contractions of the tibialis anterior (TA) muscle (100 Hz, 15 min) and treated orally with the HCE (once or three times with a fixed dose of 498 mg/kg), before and after acute exercise. Serum creatine kinase activity was determined by a kinetic method and macrophage infiltration by histological analyses of TA muscle. Lipid peroxidation was measured as malondialdehyde (MDA) levels. Nitric oxide production was evaluated by measuring nitrite formation, using Griess reagent, and nitrotyrosine was assessed by western blotting.ResultsSerum creatine kinase activities in the controls (111 U/L) increased 1 h after acute exercise (443 U/L). Acute exercise also increased the infiltration of macrophages into TA muscle; lipid peroxidation levels in TA muscle (967%), liver (55.5%) and brain (108.9%), as well as the nitrite levels by 90.5%, 30.7% and 60%, respectively. The pattern of nitrotyrosine formation was also affected by acute exercise. Treatment with HCE decreased macrophage infiltration, lipid peroxidation, nitrite production and nitrotyrosine levels to control values.ConclusionAcute exercise induced by functional electrical stimulation in rats resulted in increase in lipid peroxidation, nitrite and nitrotyrosine levels in brain, liver and skeletal muscle. The exercise protocol, that involved eccentric muscle contraction, also caused some muscle trauma, associated with over-exertion, leading to inflammation. The extract of P. emarginatus abolished most of these oxidative processes, thus confirming the high antioxidant activity of this oil which infusions are used in folk medicine against inflammatory processes.
Highlights
The aim of the present work was to evaluate the effect of a hexane crude extract (HCE) of Pterodon emarginatus on the oxidative and nitrosative stress induced in skeletal muscle, liver and brain of acutely exercised rats
The rats were allocated to six experimental groups: (1) rested control group; (2) acutely exercised group; (3) rested group treated with P. emarginatus hexane crude extract (HCE); (4) acutely exercised group treated with the P. emarginatus HCE 0.5 h before exercise, (5) acutely exercised group treated with the P. emarginatus HCE 0.5 h after exercise and (6) acutely exercised group treated with three administrations of HCE given at 24 h, 12 h and 0.5 h before exercise
EbFrfifgaeiucntr, eolivf4etrheanHdCTEAfrmoumscPl.eeamftaerrgiancaututes oexnenrictirsiete levels in Effect of the HCE from P. emarginatus on nitrite levels in brain, liver and tibialis anterior (TA) muscle after acute exercise. (A) Nitrite levels were estimated by the Griess reaction in tissue homogenates of rested control rats and at 1 h (Exer 1 h), 6 h (Exer 6 h) and 48 h (Exer 48 h) after exercise. (B) Nitrite was determined in tissue homogenates of rested control rats (1); acutely exercised rats (2); rested rats treated with HCE (3); acutely exercised rats treated with HCE 0.5 h before exercise (4) acutely exercised rats treated with HCE 0.5 h after exercise (5)
Summary
The aim of the present work was to evaluate the effect of a hexane crude extract (HCE) of Pterodon emarginatus on the oxidative and nitrosative stress induced in skeletal muscle, liver and brain of acutely exercised rats. Tissue damage resulting from acute or chronic exercise ranges from considerable fiber disruption to subcellular damage [2,3] Such damage may arise from oxidative stress caused by reactive oxygen species (ROS), which elicit different responses, depending on the organ or tissue and its levels of endogenous antioxidant [1]. In response to eccentric contraction-induced muscle damage, neutrophils and macrophages migrate to the site, infiltrate the muscle tissue, activate cytokines, and produce additional ROS [4,5]. These activities may overwhelm the natural antioxidant defenses of the cell and lead to lipid peroxidation and delayed-onset muscle damage [4,5]. Increased levels of lipid peroxidation have been detected after sprint exercise in blood samples from sprint-trained athletes [6] and in the skeletal muscle of rats after sprint and acute exercise [3,5]
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