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1: Biochem Biophys Res Commun. 2000 Sep 7;275(3):825-30.
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Geranylgeranylacetone enhances expression of thioredoxin and suppresses ethanol-induced cytotoxicity in cultured hepatocytes.

Hirota K, Nakamura H, Arai T, Ishii H, Bai J, Itoh T, Fukuda K, Yodoi J.

Department of Anesthesia, Kyoto University Hospital, Kyoto University, 54 Shogoin-Kawaharacho, Kyoto, Sakyo-Ku, 606-8507, Japan. khirota@kuhp.kyoto-u.ac.jp

Geranylgeranylacetone (GGA) has been introduced into the clinical field as an anti-ulcer drug. In addition to protective effects on gastric mucosal cells, GGA also has anti-apoptotic effects against ischemia and reperfusion injury in hepatocytes and intestinal cells. However, the molecular mechanisms of the cytoprotective or anti-apoptotic effect of GGA are largely unknown. To explore the molecular mechanism of GGA action, we focused on thioredoxin (TRX), an endogenous-redox-acting molecule. We have demonstrated that GGA induces the messenger RNA and protein of TRX and affects the activation of transcription factors, AP-1 and NF-kappaB, and that GGA blunted ethanol-induced cytotoxicity of cultured hepatocytes. These results provide evidence suggesting that a possible novel molecular mechanism of GGA is to protect cells via the induction of TRX and the activation of transcription factors such as NF-kappaB and AP-1. Copyright 2000 Academic Press.

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PMID: 10973806 [PubMed - indexed for MEDLINE]