Oxidative stress – assassin behind the ischemic stroke

Hanumanthappa, Pradeep; Joseph, Diya B.; Shashikumar, Shivaiah; Rajanikant, G. K.

doi:10.5114/fn.2012.30522

Cited by 82 publications

(68 citation statements)

References 97 publications

(102 reference statements)

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“…Oxidative stress and glutamate exposure are two of the major triggers of brain damage during ischemic stroke (Davalos et al 1997, Kostandy 2012, Pradeep et al 2012. However, exposure to high levels of glutamate (up to 0.8 mM) did not induce NPC apoptosis or necrosis as determined by Annexin V/PI staining followed by flow cytometry (Fig.…”

Section: Aag Treatment Attenuated Oxidative Stress-mediated Cell Dementioning

confidence: 99%

Low dose Hsp90 inhibitor 17AAG protects neural progenitor cells from ischemia induced death

Bradley

Zhao

Wang

et al. 2014

J. Cell Commun. Signal.

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Stress adaptation effect provides cell protection against ischemia induced apoptosis. Whether this mechanism prevents other types of cell death in stroke is not well studied. This is an important question for regenerative medicine to treat stroke since other types of cell death such as necrosis are also prominent in the stroke brain apart from apoptosis. We report here that treatment with 17-N-Allylamino-17-demethoxygeldanamycin (17AAG), an Hsp90 inhibitor, protected neural progenitor cells (NPCs) against oxygen glucose deprivation (OGD) induced cell death in a dose dependent fashion. Cell death assays indicated that 17AAG not only ameliorated apoptosis, but also necrosis mediated by OGD. This NPC protection was confirmed by exposing cells to oxidative stress, a major stress signal prevalent in the stroke brain. Mechanistic studies demonstrated that 17AAG activated PI3K/Akt and MAPK cell protective pathways. More interestingly, these two pathways were activated in vivo by 17AAG and 17AAG treatment reduced infarct volume in a middle cerebral artery occlusion (MCAO) stroke model. These data suggest that 17AAG protects cells against major cell death pathways and thus might be used as a pharmacological conditioning agent for regenerative medicine for stroke.

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Section: Aag Treatment Attenuated Oxidative Stress-mediated Cell Dementioning

confidence: 99%

Low dose Hsp90 inhibitor 17AAG protects neural progenitor cells from ischemia induced death

Bradley

Zhao

Wang

et al. 2014

J. Cell Commun. Signal.

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“…Lymphocyte subpopulation was differentiated among lysed whole blood cells, basing on correlated measurements of Forward-and Side-Scattered light (FSC and SSC) ( Fig. 1) [21].…”

Section: Flow Cytometrymentioning

confidence: 99%

“…Inflammatory and immunological factors play an important role in ischemic stroke pathogenesis, taking into consideration their involvement in an ischemic lesion development [9,21].…”

Section: Introductionmentioning

confidence: 99%

Original article Circulated CD4 + CD28 - lymphocytes rate and their cytotoxicity and morphological parameters of internal carotid artery atheromatous plaques in patients with atherosclerosis-related ischemic stroke

Masztalewicz¹,

Nowacki²,

Bajer-Czajkowska³

et al. 2013

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“…The cellular and molecular mechanisms of ischemia-evoked brain damage have been well documented. They include NMDA receptor mediated excitotoxicity, cal-cium imbalance, oxidative stress and disturbed intracellular signaling [5,14,25,50,51]. These mechanisms appear to be promising targets for therapeutic interventions.…”

Section: Introductionmentioning

confidence: 99%

Original article Delayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia

Makarewicz¹,

Sulejczak²,

Duszczyk³

et al. 2014

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A b s t r a c t Introduction: In vitro experiments have demonstrated that preconditioning primary neuronal cultures by temporary application of NMDA receptor antagonists induces long-term tolerance against lethal insults.In the present study we tested whether similar effects also occur in brain submitted to ischemia in vivo and whether the potential benefit outweighs the danger of enhancing the constitutive apoptosis in the developing brain. Material and methods: Memantine in pharmacologically relevant doses of 5 mg/kg or (+)MK-801 (3 mg/kg) was administered i.p. 24, 48, 72 and 96 h before 3-min global forebrain ischemia in adult Mongolian gerbils or prior to hypoxia/ ischemia in 7-day-old rats. Neuronal loss in the hippocampal CA1 in gerbils or weight deficit of the ischemic hemispheres in the rat pups was evaluated after 14 days. Also, the number of apoptotic neurons in the immature rat brain was evaluated. Results: In gerbils only the application of (+)MK-801 24 h before ischemia resulted in significant prevention of the loss of pyramidal neurons. In rat pups administration of (+)MK-801 at all studied times before hypoxia-ischemia

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Oxidative stress – assassin behind the ischemic stroke

Abstract: A b s t r a c t

Cited by 82 publications

References 97 publications

Low dose Hsp90 inhibitor 17AAG protects neural progenitor cells from ischemia induced death

Low dose Hsp90 inhibitor 17AAG protects neural progenitor cells from ischemia induced death

Original article Circulated CD4 + CD28 - lymphocytes rate and their cytotoxicity and morphological parameters of internal carotid artery atheromatous plaques in patients with atherosclerosis-related ischemic stroke

Original article Delayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia

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