Nrf2 Activation, an Innovative Therapeutic Alternative in Cerebral Ischemia

Silva-Islas, Carlos Alfredo; Santana-Martínez, Ricardo A.; Colín-González, Ana Laura; Maldonado, Perla D.

doi:10.5772/34324

Cited by 4 publications

(2 citation statements)

References 127 publications

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“…As mentioned above, the protective effect of DATS at the histological and motor function levels could be associated with its direct and indirect antioxidant properties since we observed a decrease in the oxidative stress; however, we focused on evaluating its indirect antioxidant properties. Indirect antioxidants induce Nrf2 activation and increase the endogenous antioxidant defense, triggering a long-term protection against oxidative stress, compared with direct antioxidants which react with ROS and are consumed, generating a short-term protection [40].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2019

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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.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2019

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“…Lee et al reported the major functional categories of genes responsible for conferring protection against oxidative stress or inflammation [ 46 ]. These genes codify for detoxifying enzymes, antioxidant proteins, NADPH-producing proteins, growth factors, defense/immune/inflammation related proteins, and signaling proteins; thus, the activation of Nrf2/ARE (antioxidant response element) pathway could stimulate a synergistic protective effect [ 47 ].…”

Section: Antioxidant Mechanisms Associated With the Protective Effmentioning

confidence: 99%

The Antioxidant Mechanisms Underlying the Aged Garlic Extract- and S-Allylcysteine-Induced Protection

Colín-González

Santana-Martínez

Silva-Islas

et al. 2012

Oxidative Medicine and Cellular Longevity

244

188

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Aged garlic extract (AGE) is an odorless garlic preparation containing S-allylcysteine (SAC) as its most abundant compound. A large number of studies have demonstrated the antioxidant activity of AGE and SAC in both in vivo—in diverse experimental animal models associated to oxidative stress—and in vitro conditions—using several methods to scavenge reactive oxygen species or to induce oxidative damage. Derived from these experiments, the protective effects of AGE and SAC have been associated with the prevention or amelioration of oxidative stress. In this work, we reviewed different antioxidant mechanisms (scavenging of free radicals and prooxidant species, induction of antioxidant enzymes, activation of Nrf2 factor, inhibition of prooxidant enzymes, and chelating effects) involved in the protective actions of AGE and SAC, thereby emphasizing their potential use as therapeutic agents. In addition, we highlight the ability of SAC to activate Nrf2 factor—a master regulator of the cellular redox state. Here, we include original data showing the ability of SAC to activate Nrf2 factor in cerebral cortex. Therefore, we conclude that the therapeutic properties of these molecules comprise cellular and molecular mechanisms at different levels.

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The Role of Nonneuronal Nrf2 Pathway in Ischemic Stroke: Damage Control and Potential Tissue Repair

Yang

Sun

Zhang

2016

Springer Series in Translational Stroke Research

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Nrf2 Activation, an Innovative Therapeutic Alternative in Cerebral Ischemia

Cited by 4 publications

References 127 publications

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

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

The Antioxidant Mechanisms Underlying the Aged Garlic Extract- and S-Allylcysteine-Induced Protection

The Role of Nonneuronal Nrf2 Pathway in Ischemic Stroke: Damage Control and Potential Tissue Repair

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