Identification of proteins in hyperglycemia and stroke animal models

Sung, Jin-Hee; Shah, Fawad Ali; Gim, Sang-Ah; Koh, Phil-Ok

doi:10.1016/j.jss.2015.07.020

Cited by 14 publications

(12 citation statements)

References 36 publications

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“…A total of 2-mm thick coronary sections were cut from the frontal lobe with a sharp blade. Slices were incubated in 2% 2,3,5-triphenyl tetrazolium chloride (TTC) for 10 to 20 min in a water bath at 37 • C until a thorough demarcation was observed, and then fixed in 4% paraformaldehyde solution and photographed (Sung et al, 2016;Shah et al, 2018). The infarct area was then measured with the ImageJ program and expressed as a percentage to the total area.…”

Section: Staining and Histological Preparationmentioning

confidence: 99%

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Potent Natural Antioxidant Carveol Attenuates MCAO-Stress Induced Oxidative, Neurodegeneration by Regulating the Nrf-2 Pathway

et al. 2020

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Ischemic stroke is a severe neurological disorder with a high prevalence rate in developed countries. It is characterized by permanent or transient cerebral ischemia and it activates syndrome of pathological events such as membrane depolarization, glutamate excitotoxicity, and intracellular calcium buildup. Carveol is widely employed as anti-inflammatory and antioxidant in traditional Chinese medicine. In the present study, the neuroprotective effects of post-treated carveol were demonstrated against transient middle cerebral artery occlusion (MCAO) induced focal ischemic cerebral injury. Male Sprague Dawley (SD) rats were subjected to two different experimental protocols to determine the dose and effects of carveol, and to demonstrate the underlying role of the nuclear factor E2-related factor (Nrf2) pathway. Our results showed that MCAO induced marked neuronal injury in the ipsilateral cortex and striatum associated with higher inflammatory cytokines expression, along with apoptotic markers such as caspase-3 and the phosphorylated c-Jun N-terminal kinase (JNK). Furthermore, MCAO induced a marked increase in oxidative stress as evidenced by high lipid peroxidase (LPO) content accompanied by the depressed antioxidant system. Carveol significantly reversed the oxidative stress and downregulated inflammatory cascades by enhancing endogenous antioxidant mechanisms including the Nrf2 gene, which critically regulates the expression of several downstream antioxidants. Further, to determine the possible involvement of Nrf2 in carveol mediated neuroprotection, we antagonized Nrf2 by alltrans retinoic acid (ATRA), and such treatment abrogated the protective effects of carveol accompanied with exaggerated neuronal toxicity as demonstrated by higher infarction area. The target effects of carveol were further supported by molecular docking analysis of drug-protein interactions. Together, our findings suggest that carveol could activate endogenous master anti-oxidant Nrf2, which further regulates the expression of downstream antioxidants, eventually ameliorating MCAO-induced neuroinflammation and neurodegeneration.

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Section: Staining and Histological Preparationmentioning

confidence: 99%

“…The number of images per slide was five per group while focusing specifically on vacuoles formation, the number of surviving neurons, and infiltrations (Shah et al, 2018). The TIFF images were optimized to the same threshold intensity for all groups (Sung et al, 2016).…”

Section: Hematoxylin Eosin (Hande) Stainingmentioning

confidence: 99%

Potent Natural Antioxidant Carveol Attenuates MCAO-Stress Induced Oxidative, Neurodegeneration by Regulating the Nrf-2 Pathway

et al. 2020

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“…Middle cerebral artery occlusion was operated as previously described method (Shah et al, 2014, 2016; Sung et al, 2016). Briefly, rats were anesthetized by mixture of xylazine and ketamine (1:3.2, I/P).…”

Section: Methodsmentioning

confidence: 99%

Melatonin Protects MCAO-Induced Neuronal Loss via NR2A Mediated Prosurvival Pathways

et al. 2019

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Stroke is the significant cause of human mortality and sufferings depending upon race and demographic location. Melatonin is a potent antioxidant that exerts protective effects in differential experimental stroke models. Several mechanisms have been previously suggested for the neuroprotective effects of melatonin in ischemic brain injury. The aim of this study is to investigate whether melatonin treatment affects the glutamate N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor signaling in cerebral cortex and striatum 24 h after permanent middle cerebral artery occlusion (MCAO). Melatonin (5 mg/kg) attenuated ischemia-induced down regulation of NMDA receptor 2 (NR2a), postsynaptic density-95 (PSD95) and increases NR2a/PSD95 complex association, which further activates the pro-survival PI3K/Akt/GSK3β pathway with mitigated collapsin response mediator protein 2 (CRMP2) phosphorylation. Furthermore, melatonin increases the expression of γ-enolase, a neurotrophic factor in ischemic cortex and striatum, and preserve the expression of presynaptic (synaptophysin and SNAP25) and postsynaptic (p-GluR1845) protein. Our study demonstrated a novel neuroprotective mechanism for melatonin in ischemic brain injury which could be a promising neuroprotective agent for the treatment of ischemic stroke.

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“…The 2-h ischemia group indicated near complete loss of ATP production, synaptic dysfunction with degraded cytoarchitecture, more conservative chaperone activity, and additional cell survival factors than those seen in the 30-min ischemia group [20]. Compared with nondiabetic MCAO rats, expression of metabolism-related enzymes, including isocitrate dehydrogenase, glyceraldehyde-3-phosphate dehydrogenase, adenosylhomocysteinase, pyruvate kinase, and glucose-6phosphate isomerase was decreased in diabetic MCAO rats, suggesting that the diabetic condition may enhance brain ischemic damage via downregulating metabolism-related protein expression [21]. In addition, the 2DE-coupled MALDI-TOF MS was used to test ischemia-induced changes in protein level in the pituitary, adrenal gland, splenic lymphocytes, hippocampus, plasma, spinal cord, and sciatic nerve [22][23][24][25].…”

Section: Tissue Proteomics Studies In Animal Ischemia Model Without Imentioning

confidence: 90%

“…Using 2DE analysis and MALDI-TOF MS, there were four studies performed in rats to tested the different protein expression in ischemic cortex between middle cerebral artery occlusion (MCAO) group and sham group at 24 h after surgery [18,19], a 30-min ischemia group and 2-h ischemia group [20], and a nondiabetic group and diabetic group [21]. Compared with sham group, upregulation of 60 kDa heat shock protein, dehydropyrimidinase-related protein 2, t-complex protein 1, Rho GDP dissociation inhibitor, spectrin alpha II chain, heat shock cognate protein 70 pseudogene 1, and tropomodulin 2 after focal cerebral ischemia in rats was proved [18,19].…”

Section: Tissue Proteomics Studies In Animal Ischemia Model Without Imentioning

confidence: 99%

Proteomic-Based Approaches for the Study of Ischemic Stroke

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et al. 2019

Transl. Stroke Res.

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Identification of proteins in hyperglycemia and stroke animal models

Cited by 14 publications

References 36 publications

Potent Natural Antioxidant Carveol Attenuates MCAO-Stress Induced Oxidative, Neurodegeneration by Regulating the Nrf-2 Pathway

Potent Natural Antioxidant Carveol Attenuates MCAO-Stress Induced Oxidative, Neurodegeneration by Regulating the Nrf-2 Pathway

Melatonin Protects MCAO-Induced Neuronal Loss via NR2A Mediated Prosurvival Pathways

Proteomic-Based Approaches for the Study of Ischemic Stroke

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