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Antioxidants (Basel). 2019 Sep 18;8(9). pii: E410. doi: 10.3390/antiox8090410.

Diallyl Trisulfide Protects Rat Brain Tissue against the Damage Induced by Ischemia-Reperfusion through the Nrf2 Pathway.

Author information

1
Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía, CDMX 14269, Mexico. charlssilv@gmail.com.
2
Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía, CDMX 14269, Mexico. echanezc@gmail.com.
3
Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México, CDMX 04510, Mexico. dianabarrera@hotmail.com.
4
Laboratorio de Patología Experimental, Instituto Nacional de Neurología y Neurocirugía, CDMX 14269, Mexico. aortizplata@yahoo.com.mx.
5
Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, CDMX 04510, Mexico. pedraza@unam.mx.
6
Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía, CDMX 14269, Mexico. maldonado.perla@gmail.com.

Abstract

Stroke is a public health problem due to its high mortality and disability rates; despite these, the pharmacological treatments are limited. Oxidative stress plays an important role in cerebral damage in stroke and the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) confers protection against oxidative stress. Different compounds, such as diallyl trisulfide (DATS), have the ability to activate Nrf2. DATS protects against the damage induced in oxygen-glucose deprivation in neuronal cells; however, in in vivo models of cerebral ischemia, DATS has not been evaluated. Male Wistar rats were subjected to 1 h of ischemia and seven days of reperfusion and the protective effect of DATS was evaluated. DATS administration (IR + DATS) decreased the infarct area and brain damage in the striatum and cortex; improved neurological function; decreased malondialdehyde and metalloproteinase-9 levels; increased Nrf2 activation in the cortex and the expression of superoxide dismutase 1 (SOD1) in the nucleus, SOD2 and glutathione S-transferase (GST) in the striatum and cortex; and increased the activity of catalase (CAT) in the striatum and glutathione peroxidase (GPx) in the cortex. Our results demonstrate the protective effect of DATS in an in vivo model of cerebral ischemia that involves Nrf2 activation.

KEYWORDS:

GST; Nrf2; SOD1; SOD2; brain; cerebral ischemia; diallyl trisulfide; ischemia-reperfusion; stroke

PMID:
31540440
DOI:
10.3390/antiox8090410
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