Vatairea macrocarpa Lectin (VML) Induces Depressive-like Behavior and Expression of Neuroinflammatory Markers in Mice

Filipe Marques Gonçalves, Andiara Espíndola Freitas, Tanara Vieira Peres, Débora Kurrle Rieger, Juliana Ben, Mariana Maestri, Ana Paula Costa, Ana Carolina Tramontina, Carlos Alberto Gonçalves, Ana Lúcia Severo Rodrigues, Celso Shiniti Nagano, Edson Holanda Teixeira, Kyria S. Nascimento, Benildo Sousa Cavada, Rodrigo Bainy Leal

Lectins are proteins capable of reversible binding to the carbohydrates in glycoconjugates that can regulate many physiological and pathological events. Galectin-1, a β-galactoside-binding lectin, is expressed in the central nervous system (CNS) and exhibits neuroprotective functions. Additionally, lectins isolated from plants have demonstrated beneficial action in the CNS. One example is a lectin with mannose-glucose affinity purified from Canavalia brasiliensis seeds, ConBr, which displays neuroprotective and antidepressant activity. On the other hand, the effects of the galactose-binding lectin isolated from Vatairea macrocarpa seeds (VML) on the CNS are largely unknown. The aim of this study was to verify if VML is able to alter neural function by evaluating signaling enzymes, glial and inflammatory proteins in adult mice hippocampus, as well as behavioral parameters. VML administered by intracerebroventricular (i.c.v) route increased the immobility time in the forced swimming test (FST) 60 min after its injection through a carbohydrate recognition domain-dependent mechanism. Furthermore, under the same conditions, VML caused an enhancement of COX-2, GFAP and S100B levels in mouse hippocampus. However, phosphorylation of Akt, GSK-3β and mitogen-activated protein kinases named ERK1/2, JNK1/2/3 and p38(MAPK), was not changed by VML. The results reported here suggest that VML may trigger neuroinflammatory response in mouse hippocampus and exhibit a depressive-like activity. Taken together, our findings indicate a dual role for galactose binding lectins in the modulation of CNS function.