Link Between Oxidative Stress and Acute Brain Ischemia

Radak, Djordje; Resanović, Ivana; Isenović, Esma R.

doi:10.1177/0003319713506516

Cited by 92 publications

(61 citation statements)

References 118 publications

(266 reference statements)

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“…The potential role of oxidative damage as a downstream process in AD pathogenesis has garnered a great deal of interest [164,165]. This interest is mainly because the brain is the most highly oxygen-metabolizing organ in the body; thus, it is highly susceptible to oxidative damage [166][167][168][169][170]. Moreover, the brain has a high lipid content that is prone to oxidation [165,167].…”

Section: Aβ Pathophysiologymentioning

confidence: 99%

The Ubiquitin-Proteasome System and Molecular Chaperone Deregulation in Alzheimer’s Disease

Sulistio

Heese

2015

Mol Neurobiol

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One of the shared hallmarks of neurodegenerative diseases is the accumulation of misfolded proteins. Therefore, it is suspected that normal proteostasis is crucial for neuronal survival in the brain and that the malfunction of this mechanism may be the underlying cause of neurodegenerative diseases. The accumulation of amyloid plaques (APs) composed of amyloid-beta peptide (Aβ) aggregates and neurofibrillary tangles (NFTs) composed of misfolded Tau proteins are the defining pathological markers of Alzheimer's disease (AD). The accumulation of these proteins indicates a faulty protein quality control in the AD brain. An impaired ubiquitin-proteasome system (UPS) could lead to negative consequences for protein regulation, including loss of function. Another pivotal mechanism for the prevention of misfolded protein accumulation is the utilization of molecular chaperones. Molecular chaperones, such as heat shock proteins (HSPs) and FK506-binding proteins (FKBPs), are highly involved in protein regulation to ensure proper folding and normal function. In this review, we elaborate on the molecular basis of AD pathophysiology using recent data, with a particular focus on the role of the UPS and molecular chaperones as the defensive mechanism against misfolded proteins that have prion-like properties. In addition, we propose a rational therapy approach based on this mechanism.

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Section: Aβ Pathophysiologymentioning

confidence: 99%

The Ubiquitin-Proteasome System and Molecular Chaperone Deregulation in Alzheimer’s Disease

Sulistio

Heese

2015

Mol Neurobiol

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“…A reduced brain damage was observed after ischemia in iNOS knockout mice and the increased expression of iNOS contributes to neuronal injury [43]. In addition, NO increases the formation of free radical and promotes brain damage after stroke by generated iNOS [44]. In this experiment, it showed that the expression of iNOS was increased in the vehicle-treated group compared with the sham-treated group.…”

Section: Discussionmentioning

confidence: 55%

Anti-inflammation Effects of Oxysophoridine on Cerebral Ischemia–Reperfusion Injury in Mice

Wang

Zhao

et al. 2015

Inflammation

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Oxysophoridine (OSR) is a bioactive alkaloid extracted from the Sophora alopecuroides Linn. Our aim is to explore the potential anti-inflammation mechanism of OSR in cerebral ischemic injury. Mice were intraperitoneally pretreated with OSR (62.5, 125, and 250 mg/kg) or nimodipine (Nim) (6 mg/kg) for 7 days followed by cerebral ischemia. The inflammatory-related cytokines in cerebral ischemic hemisphere tissue were determined by immunohistochemistry staining, Western blot and enzyme-like immunosorbent assay (ELISA). OSR-treated groups observably suppressed the nuclear factor kappa B (NF-κB), intercellular adhesion molecule-1 (ICAM-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). OSR-treated group (250 mg/kg) markedly reduced the inflammatory-related protein prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-8 (IL-8). Meanwhile, it dramatically increased the interleukin-10 (IL-10). Our study revealed that OSR protected neurons from ischemia-induced injury in mice by downregulating the proinflammatory cytokines and blocking the NF-κB pathway.

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“…23,24 It was shown that, especially superoxide, which formed in the reperfusion phase, combines with nitric oxide and forms peroxynitrite. 25 Love 19 suggested that in transient brain ischemia, free radicals and related reactive chemical species are responsible from the majority of the damage.…”

Section: + Modelmentioning

confidence: 99%