Publication: Diarylheptanoid 7-(3,4 dihydroxyphenyl)-5-hydroxy-1-phenyl-(1E)-1-heptene from Curcuma comosa Roxb. protects retinal pigment epithelial cells against oxidative stress-induced cell death
Issued Date
2011-02-01
Resource Type
ISSN
08872333
Other identifier(s)
2-s2.0-78650519024
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Mahidol University
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SCOPUS
Bibliographic Citation
Toxicology in Vitro. Vol.25, No.1 (2011), 167-176
Suggested Citation
Thunchnok Jitsanong, Kornnika Khanobdee, Pawinee Piyachaturawat, Kanokpan Wongprasert Diarylheptanoid 7-(3,4 dihydroxyphenyl)-5-hydroxy-1-phenyl-(1E)-1-heptene from Curcuma comosa Roxb. protects retinal pigment epithelial cells against oxidative stress-induced cell death. Toxicology in Vitro. Vol.25, No.1 (2011), 167-176. doi:10.1016/j.tiv.2010.10.014 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/12821
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Title
Diarylheptanoid 7-(3,4 dihydroxyphenyl)-5-hydroxy-1-phenyl-(1E)-1-heptene from Curcuma comosa Roxb. protects retinal pigment epithelial cells against oxidative stress-induced cell death
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Abstract
Chronic exposure to oxidative stress causes damage to retinal pigment epithelial cells which may lead to the development of age-related macular degeneration, the major cause of vision loss in humans. Anti-oxidants provide a natural defense against retinal cell damage. The present study was designed to evaluate the potential anti-oxidant activity and protective effect of two diarylheptanoids isolated from a medicinal herb Curcuma comosa; 7-(3,4 dihydroxyphenyl)-5-hydroxy-1-phenyl-(1E)-1-heptene (compound A), and 1,7-diphenyl-4(E),6(E)-heptadien-3-ol (compound B) against oxidative stress (H 2 O 2 )-induced human retinal pigment epithelial (APRE-19) cell death. The 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay indicated that the anti-oxidant activity (IC 50 ) of compound A was similar to that of vitamin C. Pre-treatment of ARPE-19 cells with 20μM compound A for 4h afforded greater protection against the insult from 500μM H 2 O 2 , compared to a similar protection period for compound B. Compound A lowered H 2 O 2 -induced lipid peroxidation, malondialdehyde formation and intracellular reactive oxygen species. Furthermore, compound A ameliorated the H 2 O 2 -induced decrease in anti-oxidant enzyme activities and subsequent apoptotic cell death in ARPE-19 cells in a dose and time-dependent manner. These results suggest that compound A protects ARPE-19 cells against oxidative stress, in part, by enhancing several anti-oxidant defense mechanisms. Therefore, compound A may have therapeutic potential for diseases associated with oxidative stress, particularly degenerative retinal diseases. © 2010 Elsevier Ltd.