Arachidonic acid metabolism in galactosamine/endotoxin induced acute liver injury in rats

Abstract

The changes of the levels of LTC₄, PGI₂ and TXA₂ in the liver tissue in SD rats with GalN/LPS-induced acute liver injury was studied with radioimmunoassay (RIA). As a result, 12 h after the administration of GaIN/LPS, serum AST (398±37 u), ALT (565 ±43 u) increased (P<0.001) and the concentration of TXA. (12188±588 pg/g · w · wt) in liver tissue increased significantly (P<0.001), while the content of LTC₄ (9713±3557 ng/g · w · wt) and PGI₂(1748±560 pg/g · w · wt) in liver tissue were not obviously changed (P>0.05) and the inflammatory changes of the pathological findings were observed. The improvement of serum ALT (330±168 u) (P<0.05) and AST (273±124 u) (P<0.05) and histopathological damage was observed after the administration of di-ethylcarbamazine (DEC), a LTA₄ synthesis inhibitor, the liver TXA₂ (12740±699) concentration significantly increased (P<0.001), while the levels of LTC₄ (8179±1653) and PGI₂ (2320±630) were not obviously changed. Serum ALT (536±74 u) and AST (416±41 u) (P>0.05) levels and histopathology did not change with administration of indomethacin, a cyclooxygenase inhibitor, but the liver LTC₄ (12166±1327) contents increased (P<0. 05) and TXA₂ (1868±791) reduced significantly (P<0.001). The present study suggests that arachidonic acid metabolism in rats with acute liver injury are significantly abnormal. Leukotrienes and thromboxane are important inflammatory mediators in the liver injury.

Keywords

arachidonic acid / galactosamine / endotoxin / liver injury

References

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