Chonnam Med J.
2000 Jun;36(2):209-218.
Nitric Oxide Prevents the IFN-gamma/LPS-induced Hepatocytic Cell Death in a Protein Kinase G-independent Manner
- Affiliations
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- 1Department of Microbiology, Wonkwang University School of Medicine, Iksan, Chonbuk.
- 2Department of Internal Medicine, Wonkwang University School of Medicine, Iksan, Chonbuk.
- 3Department of Surgery, Wonkwang University School of Medicine, Iksan, Chonbuk.
- 4Department of Microbiology, Chonbuk National University Medical School, Chonju, Chonbuk.
- 5Department of Surgery, Chonnam National University Medical School Kwangju.
- 6Department of Dental Pharmacology, School of Dentistry, Wonkwang University, Iksan, Chonbuk, Korea.
Abstract
- Although it has been well known that the role of LPS on liver damage is mediated through TNF-alpha, the direct cytotoxic effect of LPS on IFN-gamma-primed hepatocytes has not yet been clearly demonstrated. Here, we demonstrate that the IFN-gamma-mediated death of murine embryonic liver BNL- CL2 cells is potentiated by treatment of LPS (0.5 ug/ml). In addition, over 25 uM of sodium nitroprusside (SNP), an exogenous NO donor, significantly prevents cell death by IFN-gamma alone or IFN-gamma plus LPS (IFN-gamma/LPS) in a dose-dependent manner. In addition, SNP efficiently blocked death of BNL-CL2 cells only when it was added within 12 hr after treatment of IFN-gamma and IFN-gamma/LPS. However, potassium ferrocyanide (PFC), a structural analog of SNP, did not show any protective effect on the IFN-gamma alone or IFN-gamma/LPS-induced BNL-CL2 cell death. The preventive effect of SNP occurs in parallel with the suppression of caspase 3-like protease activation. In addition, we have demonstrated that a relatively high concentration as well as an appropriate period of exposure to NO may be critical to maintain cell viability against cytotoxicity by IFN-gamma and IFN-gamma LPS. Furthermore, the preventive effect of SNP in IFN-gamma/LPS-induced cell death is mediated by a protein kinase G (PKG)-independent manner.
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