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[The protective effect of prostaglandin E1 in experimental model of massive live cell necrosis].

Liu P, Wang Zq, J Zhang

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Abstract

The protective effect of PGE1 in mice injected with propionibacterium acnes (P.acnes) and subsequently with a small dose of lipopoly-saccharide-endotoxin (LPS) 7 days later was studied. The results of this study were as follows: (1) When PGE1 was administered one hour before the injection of LPS, the survival rate of mice was significantly higher (90%), than that of a control group (17%). No necrosis was found in the liver. (2) PGE1 suppressed the release of tumor necrosis factor (TNF) and secreted-interleukin-1 (SIL-1) in culture supernatants of P.acnes-elicited kupffer cells and membrane IL-1 (mIL-1) in kupffer cells in a dose-dependent manner in vitro. These results strongly suggest that PGE1 can prevent liver cell necrosis in the animal model and the mechanism of curative effect of PGE1 in massive liver cell necrosis may result from inhibition of the activity of TNF, sIL-1 and mIL-1 in the kupffer cells.

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The protective effect of PGE1 in mice injected with propionibacterium acnes (P.acnes) and subsequently with a small dose of lipopoly-saccharide-endotoxin (LPS) 7 days later was studied. The results of this study were as follows: (1) When PGE1 was administered one hour before the injection of LPS, the survival rate of mice was significantly higher (90%), than that of a control group (17%). No necrosis was found in the liver. (2) PGE1 suppressed the release of tumor necrosis factor (TNF) and secreted-interleukin-1 (SIL-1) in culture supernatants of P.acnes-elicited kupffer cells and membrane IL-1 (mIL-1) in kupffer cells in a dose-dependent manner in vitro. These results strongly suggest that PGE1 can prevent liver cell necrosis in the animal model and the mechanism of curative effect of PGE1 in massive liver cell necrosis may result from inhibition of the activity of TNF, sIL-1 and mIL-1 in the kupffer cells.

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Available abstract

The protective effect of PGE1 in mice injected with propionibacterium acnes (P.acnes) and subsequently with a small dose of lipopoly-saccharide-endotoxin (LPS) 7 days later was studied. The results of this study were as follows: (1) When PGE1 was administered one hour before the injection of LPS, the survival rate of mice was significantly higher (90%), than that of a control group (17%). No necrosis was found in the liver. (2) PGE1 suppressed the release of tumor necrosis factor (TNF) and secreted-interleukin-1 (SIL-1) in culture supernatants of P.acnes-elicited kupffer cells and membrane IL-1 (mIL-1) in kupffer cells in a dose-dependent manner in vitro. These results strongly suggest that PGE1 can prevent liver cell necrosis in the animal model and the mechanism of curative effect of PGE1 in massive liver cell necrosis may result from inhibition of the activity of TNF, sIL-1 and mIL-1 in the kupffer cells.

Key concepts: Propionibacterium acnes, Tumor necrosis factor alpha, Medicine, Necrosis, Kupffer cell, Cytokine, Prostaglandin E, In vitro

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