Hyperoside prevents oxidative damage induced by hydrogen peroxide in lung fibroblast cells via an antioxidant effect

Mei Jing Piao, Kyoung Ah Kang, Rui Zhang, Dong Ok Ko, Zhi Hong Wang, Ho Jin You, Hee Sun Kim, Ju Sun Kim, Sam Sik Kang, Jin Won Hyun

Research output: Contribution to journalArticlepeer-review

106 Scopus citations


We elucidated the cytoprotective effects of hyperoside (quercetin-3-O-galactoside) against hydrogen peroxide (H2O2)-induced cell damage. We found that hyperoside scavenged the intracellular reactive oxygen species (ROS) detected by fluorescence spectrometry, flow cytometry, and confocal microscopy. In addition, we found that hyperoside scavenged the hydroxyl radicals generated by the Fenton reaction (FeSO4 + H2O2) in a cell-free system, which was detected by electron spin resonance (ESR) spectrometry. Hyperoside was found to inhibit H2O2-induced apoptosis in Chinese hamster lung fibroblast (V79-4) cells, as shown by decreased apoptotic nuclear fragmentation, decreased sub-G1 cell population, and decreased DNA fragmentation. In addition, hyperoside pretreatment inhibited the H2O2-induced activation of caspase-3 measured in terms of levels of cleaved caspase-3. Hyperoside prevented H2O2-induced lipid peroxidation as well as protein carbonyl. In addition, hyperoside prevented the H2O2-induced cellular DNA damage, which was established by comet tail, and phospho histone H2A.X expression. Furthermore, hyperoside increased the catalase and glutathione peroxidase activities. Conversely, the catalase inhibitor abolished the cytoprotective effect of hyperoside from H2O2-induced cell damage. In conclusion, hyperoside was shown to possess cytoprotective properties against oxidative stress by scavenging intracellular ROS and enhancing antioxidant enzyme activity.

Original languageEnglish
Pages (from-to)1448-1457
Number of pages10
JournalBiochimica et Biophysica Acta - General Subjects
Issue number12
StatePublished - Dec 2008

Bibliographical note

Funding Information:
This research was supported by the DNA repair regulation with disease program [M1063901] of the Korea Science and Engineering Foundation (KOSEF) and by the program of Basic Atomic Energy Research Institute (BAERI) which is a part of the Nuclear R and D programs grant from the Ministry of Science and Technology of Korea.


  • Apoptosis
  • DNA damage
  • Hyperoside
  • Lipid peroxidation
  • Protein carbonyl
  • Reactive oxygen species


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