The salutary Nrf2-dependent attenuation of reactive gliosis may contribute to this neuroprotection, offering new insight into the cellular basis of an Nrf2-targeting strategy for stroke prevention or treatment.
This review outlines the literature for Nrf2 studies in preclinical stroke and focuses on the <i>in vivo</i> evidence for the role of Nrf2 in primary and secondary brain injuries.
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.
The nuclear factor erythroid-2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway plays a key role in inducing phase II detoxifying enzymes and antioxidant proteins and is now considered as a interesting therapeutic target for the treatment of stroke.
Together, Ginseng pretreatment protects against acute sensorimotor deficits and promotes its long-term recovery after pdMCAO, at least partly, through Nrf2 activation, highlighting the potential efficacy of oral consumption of Ginseng for stroke preventative intervention in patients who are at great risk of recurrent stroke or transient ischemic attack.
Our findings indicated that treatment with genistein could alleviated oxidative stress injury induced by cerebral ischemia in ovariectomized rats via promoting Nrf2 and NQO1 expression, which provide a new molecular mechanism for the neuroprotective effects of genistein against stroke in postmenopausal women.
Our study provides proof of concept for the modulation of Nrf2, so as to tilt the balance toward angiogenesis, representing a therapeutic strategy for hypoxia or ischemia disorders such as stroke.
The information presented here may be useful in the design of future experimental research and increase the likelihood of using Nrf2 as a therapeutic target for stroke in the future.
Together, intranasal delivery of Z-LIG enhanced protection against ischemic injury via Nrf2 and HSP70 signaling pathways and has prophylactic potential in the population at high risk of stroke.
Recently published in vitro and in vivo findings strongly suggest that BBB impairment and increased risk for stroke by tobacco smoke (TS) closely resemble that of type-2 diabetes (2DM) and develop largely in response to common key modulators such oxidative stress (OS), inflammation and alterations of the endogenous antioxidative response system (ARE) regulated by the nuclear factor erythroid 2-related factor (Nrf2).
The main purpose of this review is to discuss the current evidence for the role of Nrf2 in stroke and the potential interventions to enhance Nrf2 activation to attenuate stroke-induced injury.
Exploiting the dual action of natural Nrf2 inducers may provide a novel therapeutic strategy for restoring cellular redox homeostasis in aging and cardiovascular related diseases such diabetes, atherosclerosis and stroke.