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Literature DB >> 21371450

2-Ethoxy-4,5-diphenyl-1,3-oxazine-6-one activates the Nrf2/HO-1 axis and protects against oxidative stress-induced neuronal death.

Niloufar Ansari¹, Fariba Khodagholi, Mohsen Amini.

Abstract

Apoptosis or programmed cell death has been suggested as an important mode of neurodegeneration in Alzheimer's disease pathogenesis. The present study explored the neuroprotective effect of 2-ethoxy-4,5-diphenyl-1,3-oxazine-6-one (EDPOO) against H(2)O(2)-induced cell death in rat pheochromocytoma (PC12) cells. We found that H(2)O(2) triggered a range of cellular cascades which leads to cell death, whereas pretreatment of the cells with this oxazine derivative attenuated the extent of apoptosis, as assessed by MTT assay, acridine orange/ethidium bromide staining and caspase-3 expression assay. We further showed that EDPOO exerts its neuroprotective effect by enhancing Hsp-70 level, stabilizing Nrf2 and upregulation of HO-1 and γ-GCS. Moreover, this oxazine derivative regulated cellular redox status via antioxidant enzyme upregulation. The neuroprotective effect of this compound may provide a new potential application for the treatment of neurodegenerative diseases.

Entities: Chemical Disease Gene Species

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Year: 2011 PMID： 21371450 DOI： 10.1016/j.ejphar.2011.02.028

Source DB: PubMed Journal: Eur J Pharmacol ISSN： 0014-2999 Impact factor: 4.432

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Cited

10 in total

1. S. choloroleuca, S. mirzayanii and S. santolinifolia protect PC12 cells from H(2)O (2)-induced apoptosis by blocking the intrinsic pathway.

Authors: Shabnam Zeighamy Alamdary; Fariba Khodagholi; Fatemeh Shaerzadeh; Niloufar Ansari; Ali Sonboli; Solaleh Khoramian Tusi
Journal: Cytotechnology Date: 2011-12-31 Impact factor: 2.058

2. Involvement of molecular chaperones and the transcription factor Nrf2 in neuroprotection mediated by para-substituted-4,5-diaryl-3-thiomethyl-1,2,4-triazines.

Authors: Fariba Khodagholi; Niloufar Ansari; Mohsen Amini; Solaleh Khoramian Tusi
Journal: Cell Stress Chaperones Date: 2012-01-04 Impact factor: 3.667

Review 3. Targeting urate to reduce oxidative stress in Parkinson disease.

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4. Oxidative cytotoxic agent withaferin A resensitizes temozolomide-resistant glioblastomas via MGMT depletion and induces apoptosis through Akt/mTOR pathway inhibitory modulation.

Authors: Patrick T Grogan; Jann N Sarkaria; Barbara N Timmermann; Mark S Cohen
Journal: Invest New Drugs Date: 2014-04-10 Impact factor: 3.850

5. Cytotoxicity of withaferin A in glioblastomas involves induction of an oxidative stress-mediated heat shock response while altering Akt/mTOR and MAPK signaling pathways.

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10 in total

2-Ethoxy-4,5-diphenyl-1,3-oxazine-6-one activates the Nrf2/HO-1 axis and protects against oxidative stress-induced neuronal death.

1. S. choloroleuca, S. mirzayanii and S. santolinifolia protect PC12 cells from H(2)O (2)-induced apoptosis by blocking the intrinsic pathway.

2. Involvement of molecular chaperones and the transcription factor Nrf2 in neuroprotection mediated by para-substituted-4,5-diaryl-3-thiomethyl-1,2,4-triazines.

Review 3. Targeting urate to reduce oxidative stress in Parkinson disease.

4. Oxidative cytotoxic agent withaferin A resensitizes temozolomide-resistant glioblastomas via MGMT depletion and induces apoptosis through Akt/mTOR pathway inhibitory modulation.

5. Cytotoxicity of withaferin A in glioblastomas involves induction of an oxidative stress-mediated heat shock response while altering Akt/mTOR and MAPK signaling pathways.

Review 6. Oxidative stress in neurodegenerative diseases: mechanisms and therapeutic perspectives.

7. Natural products as promising drug candidates for the treatment of Alzheimer's disease: molecular mechanism aspect.

8. Nrf2 signaling contributes to the neuroprotective effects of urate against 6-OHDA toxicity.

Review 9. Neuroprotective and Cognitive Enhancement Potentials of Angelica gigas Nakai Root: A Review.

Review 10. p62-Keap1-NRF2-ARE Pathway: A Contentious Player for Selective Targeting of Autophagy, Oxidative Stress and Mitochondrial Dysfunction in Prion Diseases.