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Induction of heme oxygenase-1 by Ginkgo Biloba Extract but not its terpenoids partially mediated its protective effect against lysophosphatidylcholine-induced damage

Pharmacological Research
Publication Date
DOI: 10.1006/phrs.2000.0753
  • Heme Oxygenase
  • Ginkgo Biloba Extract
  • Terpenoid Constituents
  • Lysophosphatidylcholine (Lpc)
  • Zinc Protoporphyrin-Ix (Znpp-Ix)
  • Glutathione
  • Biology


Abstract In this study, we examined whether Ginkgo Biloba Extract and its terpenoid constituents protect against oxidative stress through actions on heme oxygenase (HO) gene expression and activity. HO-1 and glutathione peroxidase (GPx) gene expressions were examined by reverse transcription polymerase chain reaction (RT-PCR) analysis, HO activity and GPx enzyme activity were analysed by spectrophotometric assay. Pretreatment of H9c2 myocytes with 100–500 μ gml −1 Ginkgo Biloba Extract caused induction of HO-1 gene expression and a significant increase in HO activity; 30 μ gml −1 ginkgolide B and 30 μ gml −1 bilobalide had little effect. Treatment with Ginkgo Biloba Extract for 24 h also significantly increased GPx gene expression and GPx enzyme activity. Pretreatment with Ginkgo Biloba Extract, ginkgolide B and bilobalide protected myocytes against lysophosphatidylcholine (LPC)-induced damage. The protective effect of Ginkgo Biloba Extract against LPC-induced damage was partially suppressed by a HO inhibitor, Zinc protoporphyrin-IX (ZnPP-IX), while ZnPP-IX did not suppress the protective effect of ginkgolide B or bilobalide. Furthermore, pretreatment with hemin, biliverdin or bilirubin reduced cytotoxicity induced by LPC. These results suggest that induction of HO-1 by Ginkgo Biloba Extract but not its terpenoid constituents may play a beneficial role in oxidative stress. The mechanism of Ginkgo Biloba Extract-induced HO-1 gene expression and the increase in HO activity may be related to alteration of intracellular glutathione levels.

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