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https://www.arca.fiocruz.br/handle/icict/20597
1,8-CINEOLE PROTECTS AGAINST LIVER FAILURE IN AN IN-VIVO MURINE MODEL OF ENDOTOXEMIC SHOCK
Author
Affilliation
Federal University of Ceará. Department of Physiology and Pharmacology. Fortaleza, CE, Brasil
Federal University of Ceará. Department of Physiology and Pharmacology. Fortaleza, CE, Brasil
Federal University of Ceará. Department of Physiology and Pharmacology. Fortaleza, CE, Brasil
Federal University of Ceará. Department of Physiology and Pharmacology. Fortaleza, CE, Brasil
Federal University of Ceará. Department of Pathology and Legal Medicine. Fortaleza,
Federal University of Ceará. Department of Pathology and Legal Medicine. Fortaleza,
Fundação Oswaldo Cruz. Laboratório de Patologia e Biologia Celular. Rio de Janeiro, RJ, Brasil
Fundação Oswaldo Cruz. Laboratório de Patologia e Biologia Celular. Rio de Janeiro, RJ, Brasil
Federal University of Ceará. Department of Physiology and Pharmacology. Fortaleza, CE, Brasil
Federal University of Ceará. Department of Physiology and Pharmacology. Fortaleza, CE, Brasil
Federal University of Ceará. Department of Physiology and Pharmacology. Fortaleza, CE, Brasil
Federal University of Ceará. Department of Pathology and Legal Medicine. Fortaleza,
Federal University of Ceará. Department of Pathology and Legal Medicine. Fortaleza,
Fundação Oswaldo Cruz. Laboratório de Patologia e Biologia Celular. Rio de Janeiro, RJ, Brasil
Fundação Oswaldo Cruz. Laboratório de Patologia e Biologia Celular. Rio de Janeiro, RJ, Brasil
Abstract
The effects of 1,8-cineole on D-galactosamine/lipopolysaccharide (GalN/LPS)-induced shock
model of liver injury was investigated in mice. The co-administration of GalN (700 mg kg−1, i.p.)
and LPS (5 lgkg−1, i.p.) greatly elevated serum concentrations of tumour necrosis factor-a (TNFa),
alanine aminotransferase and aspartate aminotransferase, and induced massive hepatic
necrosis and lethality in 100% of control mice. Pretreatment with 1,8-cineole (400 mg kg−1,
p.o.) and dexamethasone (1 mgkg−1, s.c.), 60 min before GalN/LPS, offered complete protection
(100%) against the lethal shock and acute elevation in serum TNF-a and serum transaminases.
Hepatic necrosis induced by GalN/LPS was also greatly reduced by both 1,8-cineole and
dexamethasone treatment. The results indicate that 1,8-cineole protects mice against GalN/LPSinduced
liver injury through the inhibition of TNF-a production, and suggest that 1,8-cineole
may be a promising agent to combat septic-shock-associated pathologies.
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