Diallyl Trisulfide Protects Rat Brain Tissue against the Damage Induced by Ischemia-Reperfusion through the Nrf2 Pathway
SOD2
Diallyl trisulfide
DOI:
10.3390/antiox8090410
Publication Date:
2019-09-18T15:01:15Z
AUTHORS (6)
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 stroke activation of nuclear factor erythroid 2-related 2 (Nrf2) confers protection against oxidative stress. Different compounds, such as diallyl trisulfide (DATS), have ability activate Nrf2. DATS protects induced oxygen-glucose deprivation neuronal cells; however, vivo models ischemia, has not been evaluated. Male Wistar rats were subjected 1 h ischemia seven days reperfusion protective effect was administration (IR + DATS) decreased infarct area brain striatum cortex; improved neurological function; malondialdehyde metalloproteinase-9 levels; increased Nrf2 cortex expression superoxide dismutase (SOD1) nucleus, SOD2 glutathione S-transferase (GST) activity catalase (CAT) peroxidase (GPx) cortex. Our results demonstrate model that involves activation.
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