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Reduction of monocrotaline‐induced hepatic injury by deleted variant of hepatocyte growth factor (dHGF) in rats
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Abstract: Background: Monocrotaline is a hepatotoxic agent which exerts predominant toxicity to central veins and centrilobular sinusoids. In this study, we investigated the effects of deleted variant of hepatocyte growth factor (dHGF) on monocrotaline‐induced hepatic injury in rats. Methods: 100 mg/kg monocrotaline was gavaged to male rats twice with a 4‐days' interval. Treatment of dHGF was started 4 days before the initial administration of monocrotaline and 500μg/kg was intravenously injected twice daily for 11 days. Results: Monocrotaline induced severe damage of central veins and destruction of central zone of hepatic lobules concurrent with derangement of blood levels of total protein, albumin, alanine‐aminotransferase, total bilirubin, direct bilirubin, and hepaplastin time. dHGF reduced the structural and blood‐chemical abnormalities induced by monocrotaline. Conclusions: These results suggest that dHGF prevented and repaired the monocrotaline‐induced hepatic injury, and could have therapeutic potency in hepatic failure with sever centrilobular destruction.
Title: Reduction of monocrotaline‐induced hepatic injury by deleted variant of hepatocyte growth factor (dHGF) in rats
Description:
Abstract: Background: Monocrotaline is a hepatotoxic agent which exerts predominant toxicity to central veins and centrilobular sinusoids.
In this study, we investigated the effects of deleted variant of hepatocyte growth factor (dHGF) on monocrotaline‐induced hepatic injury in rats.
Methods: 100 mg/kg monocrotaline was gavaged to male rats twice with a 4‐days' interval.
Treatment of dHGF was started 4 days before the initial administration of monocrotaline and 500μg/kg was intravenously injected twice daily for 11 days.
Results: Monocrotaline induced severe damage of central veins and destruction of central zone of hepatic lobules concurrent with derangement of blood levels of total protein, albumin, alanine‐aminotransferase, total bilirubin, direct bilirubin, and hepaplastin time.
dHGF reduced the structural and blood‐chemical abnormalities induced by monocrotaline.
Conclusions: These results suggest that dHGF prevented and repaired the monocrotaline‐induced hepatic injury, and could have therapeutic potency in hepatic failure with sever centrilobular destruction.
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