Schinus terebinthifolius Raddi (Brazilian pepper) leaves extract: in vitro and in vivo evidence of anti-inflammatory and antioxidant properties.

The aim of this work was to evaluate the anti-inflammatory and antioxidant effects of ethyl acetate extract obtained from the leaves of Brazilian peppertree Schinus terebinthifolius Raddi (EAELSt). Total phenols and flavonoids, chemical constituents, in vitro antioxidant activity (DPPH and lipoperoxidation assays), and cytotoxicity in L929 fibroblasts were determined. In vivo anti-inflammatory and antioxidant properties were evaluated using TPA-induced ear inflammation model in mice. Phenol and flavonoid contents were 19.2 ± 0.4 and 93.8 ± 5.2 of gallic acid or quercetin equivalents/g, respectively. LC-MS analysis identified 43 compounds, of which myricetin-O-pentoside and quercetin-O-rhamnoside were major peaks of chromatogram. Incubation with EAELSt decreased the amount of DPPH radical (EC50 of 54.5 ± 2.4 µg/mL) and lipoperoxidation at 200-500 µg/mL. The incubation with EAELSt did not change fibroblast viability up to 100 µg/mL. Topical treatment with EAELSt significantly reduced edema and myeloperoxidase activity at 0.3, 1, and 3 mg/ear when compared to the vehicle-treated group. In addition, EAELSt decreased IL-6 and TNF-α levels and increased IL-10 levels. Besides, it modulated markers of oxidative stress (reduced total hydroperoxides and increased sulfhydryl contents and ferrium reduction potential) and increased the activity of catalase and superoxide dismutase, without altering GPx activity.

Does Croton Argyrophyllus Extract Has an Effect on Muscle Damage and Lipid Peroxidation in Rats Submitted to High Intensity Strength Exercise?

Many species of the genus Croton have been used for anti-inflammatory, antiproliferative, antidiabetic, and antitumor purposes. The objective was to evaluate the effect of a hydroethanolic extract (HEE) from the inner bark of Croton argyrophyllus (Euphorbiaceae) on muscle damage and oxidative stress in rats after high intensity exercise. The animals were divided into four groups: (i) the sedentary group (SV; n = 7), (ii) the exercise vehicle group (EV, n = 7), (iii) the sedentary group HEE (SHG; n = 7) composed of sedentary animals and treated with the hydroethanolic extract of C. argyrophyllus (200 mg/kg, v.o.), and (iv) the HEE exercise group (HEE; n = 7) composed of animals submitted to resistance exercise (RE) and treated with the hydroethanolic extract of C. argyrophyllus (200 mg/kg, v.o.). In the 2,2-Diphenyl-1-picrylhydrazyl (DPPH) test, the HEE showed lower values of inhibition potential (IP%) at 39.79% compared to gallic acid, 87.61%, and lipoperoxidation inhibition at 27.4% (100 µg/mL) or 28.6% (200 µg/mL) (p < 0.001). There was inhibition in free radicals in vivo. The HEE of C. argyrophyllus partially reduced the biomarkers of oxidative stress in muscle tissue and muscular damage (creatine kinase (CK) and Lactate Dehydrogenase (LDH)) (p < 0.05) in rats, and in this sense it can be an aid to the recovery process after exhaustive efforts.

In vitro and ex vivo anticholinesterase activities of Erythrina velutina leaf extracts.

CONTEXT: Erythrina velutina (EV) Willd (Fabaceae-Faboideae) is a medicinal tree that is commonly used in Brazil for the treatment of several central nervous system disorders. OBJECTIVE: The anticholinesterase activity of EV is described in this work. METHODS: Concentration-response curves (0-1.6 mg/mL) for EV leaf aqueous extract (AE) and alkaloid-rich extracts (AKEs) were performed in vitro. Cholinesterase inhibition was examined in mouse brains, as the cholinesterase source, and in pure acetylcholinesterase (AChE) or butyrylcholinesterase (BuChE). Mice were treated with AE or AKE (100, 200, and 400 mg/kg, p.o.) and their brains were used for the measurement of cholinesterase activity (CA) ex vivo. RESULTS: CA was inhibited by AE (IC(50) = 0.57 [0.43-0.75] mg/mL) and AKE (IC(50) = 0.52 [0.39-0.70] mg/mL) in brain homogenates in a concentration-dependent manner. The ex vivo experiments indicated that AE (400 mg/kg, p < 0.05, 32.2 ± 3.9% of inhibition) and AKE (all doses: p < 0.05-p < 0.001, 29.6 ± 3.2% as the maximum inhibition) significantly inhibited CA in the central nervous system after oral administration. AE and AKE inhibited AChE and BuChE activities in a concentration-dependent manner (AE: IC(50AChE) = 0.56 [0.38-0.81] mg/mL, IC(50BuChE) = 2.95 [1.51-5.76] mg/mL, AKE: IC(50AChE) = 0.87 [0.60-12.5] mg/mL, IC(50BuChE) = 2.67 [0.87-8.11] mg/mL). DISCUSSION AND CONCLUSIONS: These data indicated that AE and AKE crossed the blood-brain barrier to inhibit CA in the brain. AE and AKE also exhibited a dual inhibitory action on acetyl- and BuChE.