Open Access

ARTICLE

Allicin neuroprotective effect during oxidative/inflammatory injury involves AT1-Hsp70-iNOS counterbalance axis

LUCIANA MAZZEI^1,2, MARÍA BELÉN RUIZ-ROSO³, NATALIA DE LAS HERAS³, SANDRA BALLESTEROS³, CAROLINA TORRESPALAZZOLO⁴, LEÓN FERDER⁵, ALEJANDRA BEATRIZ CAMARGO⁴, WALTER MANUCHA^1,2,*

1 Instituto de Medicina y Biología Experimental de Cuyo (IMBECU), Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET), Mendoza, 5500, Argentina
2 Área de Farmacología, Departamento de Patología, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo Centro Universitario, Mendoza, 5500, Argentina
3 Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid, 34523, España
4 IBAM, Universidad Nacional de Cuyo, CONICET, Facultad de Ciencias Agrarias, Mendoza, M5528AHB, Argentina
5 Department of Pediatrics, Nephrology Division, Miller School of Medicine, University of Miami, Miami, 33012, USA

* Address correspondence to: Walter Manucha,

BIOCELL 2020, 44(4), 671-681. https://doi.org/10.32604/biocell.2020.014175

Received 06 September 2020; Accepted 13 October 2020; Issue published 24 December 2020

Abstract

The ancestral cultures have described many therapeutic properties of garlic; therefore, it is of central interest to elucidate the molecular basis explaining this millenary empirical knowledge. Indeed, it has been demonstrated a neuroprotective effect of allicin–a phytochemical present in garlic- linked to oxidative-inflammatory modulation. Allicin improved neuronal injury by heat shock protein 70 (Hsp70) and inducible nitric oxide synthase (iNOS) regulation. Also, allicin exerts renal protection involving a possible angiotensin type 1 receptor (AT1) interaction. In connection, AT1 overexpression has been recognized as a central deleterious factor in many brain diseases. However, there are no studies that evaluate AT1-Hsp70-iNOS interaction as a mechanism linked to neuroinflammation. Thus, our central aim is to evaluate if the allicin protective effect is associated with an AT1-Hsp70-iNOS counterbalance axis. For this study, a murine microglial cell line (BV-2) was injured with lipopolysaccharides and treated or not with allicin. Then, it was evaluated cell viability, proinflammatory cytokine levels, cellular oxidative stress, iNOS, Hsp70, and AT1 protein expression (cellular and mitochondrial fractions), nitrite levels, and protein-protein interactions. The results demonstrated that allicin could prevent neuronal injury due to a reduction in oxidative stress and inflammatory status mediated by an AT1-Hsp70-iNOS counterbalance axis linked to direct protein-protein interaction.

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