The effects of 1,8-cineole on D-galactosamine/lipopolysaccharide (GalN/LPS)
-induced shock model of liver injury was investigated in mice, The co-admin
istration of GalN (700 mg kg(-1), i.p.) and LPS (5 mug kg(-1), i.p.) greatl
y elevated serum concentrations of tumour necrosis factor-alpha (TNF-alpha)
, alanine aminotransferase and aspartate aminotransferase, and induced mass
ive hepatic necrosis and lethality in 100% of control mice. Pretreatment wi
th 1,8-cineole (400 mo kg(-1), p.o.) and dexamethasone (l mg kg(-1), s.c.),
60 min before GalN/LPS, offered complete protection (100 %) against the le
thal shock and acute elevation in serum TNF-alpha and serum transaminases.
Hepatic necrosis induced by GalN/LPS was also greatly reduced by both 1,8-c
ineole and dexamethasone treatment. The results indicate that 1,8-cineole p
rotects mice against GalN/LPS- induced liver injury through the inhibition
of TNF-alpha production, and suggest that 1,8-cineole may be a promising ag
ent to combat septic-shock-associated pathologies.