The anticonvulsant effect of a polysaccharide-rich extract from Genipa americana leaves is mediated by GABA receptor

Publication date: May 2018
Source:Biomedicine & Pharmacotherapy, Volume 101
Author(s): Dayanne Terra Tenório Nonato, Silvânia Maria Mendes Vasconcelos, Mário Rogério Lima Mota, Paulo Goberlânio de Barros Silva, Arcelina Pacheco Cunha, Nágila Maria Pontes Silva Ricardo, Maria Gonçalves Pereira, Ana Maria Sampaio Assreuy, Edna Maria Camelo Chaves
BackgroundThis study aimed to chemically characterize a polysaccharide-rich extract (PRE) obtained from Genipa americana leaves and evaluate its neuroprotective effect in the brain morphology and oxidative markers using mice behavioral models.MethodsDry powder (5 g) of G. americana leaves were submitted to depigmentation in methanol. PRE was obtained by extraction in NaOH and precipitation with absolute ethanol and characterized by infrared spectroscopy (FTIR) and nuclear magnetic resonance (¹H and ¹³C NMR). Swiss mice (25–35 g) received saline (0.9% NaCl) or PRE (1–27 mg/kg) by intraperitoneal (i.p.) route, 30 min before evaluation in behavioral models (open field, elevated plus maze, sleeping time, tail suspension, forced swimming, seizures induced by pentylenetetrazole-PTZ). Animal's brain were dissected and analyzed for histological alterations and oxidative stress.ResultsFTIR spectrum showed bands around 3417 cm⁻¹ and 2928 cm⁻¹, relative to the vibrational stretching of OH and CH, respectively. ¹H NMR spectrum revealed signals at δ 3.85 (methoxyl groups) and δ 2.4 (acetyl) ppm. ¹³C NMR spectrum revealed signals at δ 108.0 and δ 61.5 ppm, corresponding to C1 and C5 of α-L-arabinofuranosyl residues. PRE presented central inhibitory effect, increasing the latency for PTZ-induced seizures by 63% (9 mg/kg) and 55% (27 mg/kg), and the latency to death by 73% (9 mg/kg) and 72% (27 mg/kg). Both effects were reversed by the association with flumazenil.ConclusionsPRE, containing a heteropolysaccharide, presents antioxidant and anticonvulsant effect in the model of PTZ-induced seizures via gamma-aminobutyric acid (GABA), decreasing the number of hippocampal black neurons.

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