Effects of standard ethanolic extract from Erythrina velutina in acute cerebral ischemia in mice

• Published in: Biomedicine & pharmacotherapy 2017-12, Vol.96, p.1230-1239
• Main Authors: Rodrigues, Francisca Taciana Sousa, de Sousa, Caren Nádia Soares, Ximenes, Naiara Coelho, Almeida, Anália Barbosa, Cabral, Lucas Moraes, Patrocínio, Cláudio Felipe Vasconcelos, Silva, Aline Holanda, Leal, Luzia Kalyne Almeida Moreira, Honório Júnior, José Eduardo Ribeiro, Macedo, Danielle, Vasconcelos, Silvânia Maria Mendes
• Format: Article
• Language: English
• Subjects: Amino Acids - metabolism; Animals; Brain - drug effects; Brain Ischemia - drug therapy; Brain Ischemia - metabolism; Cerebral Infarction - drug therapy; Cerebral Infarction - metabolism; Cerebral Ischemia; Erythrina - chemistry; Erytrhina velutina; Ethanol - chemistry; Male; Memory - drug effects; Mice; Neuroprotection; Neuroprotective Agents - pharmacology; Plant Extracts - pharmacology
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2017.11.093

The objective of this study was to verify a possible neuroprotective effect of the ethanolic extract of Erythrina velutina (EEEV). Male Swiss mice were submitted to transient cerebral ischemia by occlusion of both carotid arteries for 30 min and treated for 5 days with EEEV (200 or 400 mg/kg) or Memantine (MEM) 10 mg/kg, with initiation of treatment 2 or 24 h after Ischemia. On the 6th day after the induction of ischemia, the animals were submitted to evaluation of locomotor activity and memory and then sacrificed. The brains were dissected for the removal of the prefrontal cortex (PFC), hippocampus (HC) and striatum (ST) for determination of amino acid concentrations. In the step down and Y-maze tests, ischemia caused damage to the animals and treatment with EEEV or MEM reversed this effect. The animals submitted to ischemia also showed memory deficit in the object recognition test, an effect that was reverted by EEEV400 and MEM10. Amino acid dosage showed an increase in excitatory amino acid concentrations in the PFC of the ischemic animals and this effect was reversed by the treatment with EEEV400/24H. Regarding the inhibitory amino acids, ischemia caused an increase of taurine in the PFC while treatment with MEM10/24H or EEEV400/24H reversed this effect. In HC, an increase in excitatory amino acids was also observed in ischemiated animals having treatment with EEEV200/2H or EEEV400/24H reversed this effect. Similar effect was also observed in the same area in relation to the inhibitory amino acids with treatment with MEM10/24H or EEEV400/24H. In the ST, ischemia was also able to cause an increase in excitatory amino acids that was reversed more efficiently by the treatments with MEM10/24H and EEEV200. Also in this area, an increase of taurine and GABA was observed and only the treatment with EEEV200/2H showed a reversion of this effect. In view of these findings, EEEV presents a neuroprotective effect possibly due to its action on amino acid concentrations, and is therefore a potential therapeutic tool in reducing the damage caused by ischemia.