Ellagic components from Caesalpinia paraguariensis (Burk.) inhibited the α-Glucosidase activity

SGARIGILA, M. A.; SOMAINI, G.C.; SOBERÓN , J.R.; JIMENEZ, C.M.; SAMPIETRO D. A.; VATTUONE, M.A.

Birmingham

Congreso; 3rd International Conference and Exhibition on Traditional & Alternative Medicine. OMICS Group International.; 2015

OMICS Group International

Caesalpinia paraguariensis is a native tree from Argentine, which it has medicinal uses. People intakes the bark infusion to improve the diabetes and decreasing the blood cholesterol level. One of the therapeutic approaches for the control of postprandial hyperglycemia is to retard glucose absorption by inhibiting carbohydrate-hydrolyzing enzymes such as α-Glucosidase (AGH) in the digestive organs. In previous works it was showed the in vivo hypoglycemic activity, as well as the phytochemical characterization for this extract indicating the presence of ellagic derivatives. This study seeks to provide evidence about relationship between ellagic components from C. paraguariensis bark infusion (CPBI) and its hypoglycemic activity, aiming at the AGH target. For this, ellagic-rich fraction (ERF) was obtained from 100 mg lyophilized CPBI, applying solid/liquid-liquid conventional methods, using aqueous and organic phases (n-butanol). ERF components were characterized by analytical RP-HPLC (Sgariglia et al., 2013). The AGH (E.C. 3.2.1.20, Saccharomyces, Sigma Co.) enzyme inhibition assay was performed according to Matsu et al. (1996). The enzyme inhibition was measured spectrophotometrically (400 nm) through monitoring of the p-nitrophenyl produced from hydrolysis of p-nitrophenyl-α-D-glucopyranoside (PNP-G) (0.7mM) by AGH (16 mU), at 37 °C, 30 min. Ellagic acid and 3-O-methylellagic acid were used as positive controls. ERF, 3-O-EA and EA reached 50 %I of AGH at ≤ 1.50 µg/ml concentrations (1.22>> 0.09>0.07, respectively), and 90%I at ≤ 4.00 µg/ml; logarithmic trends were observed, and the kinetic assays suggested a competitive type inhibition; therefore AGH would be a likely target to explain the effect of CPBI in patients.