ORY supplementation mitigates acetaminophen-induced acute liver failure in male mice: role of oxidative stress and apoptotic markers.
Marcelo Gomes De GomesLucian Del FabbroAndré Rossito GoesLeandro Cattelan SouzaSilvana Peterini BoeiraCristiano Ricardo JessePublished in: Naunyn-Schmiedeberg's archives of pharmacology (2020)
The aim of the present study was to assess the possible protective effect of γ-oryzanol (ORY) supplementation in a model of acute liver failure (ALF) induced by acetaminophen (APAP) in mice. Male Swiss strain mice were supplemented with ORY (10 and 50 mg/kg, per oral route) daily for 7 days. One hour after the last supplementation, animals received APAP (300 mg/kg, intraperitoneal). Twenty-four hours after APAP administration, mice were euthanized, and biochemical and histopathological determinations were performed. Histopathological analysis revealed that APAP caused vascular congestion, loss of cellular structure, and cellular infiltration in hepatocytes. Moreover, it caused oxidative damage (enzymatic and non-enzymatic analysis of oxidative stress), with loss of hepatic function leading to cell apoptosis (apoptotic parameters). ORY supplementation (ORY-10 and ORY-50) protected against all changes in ALF model. Thus, the protective effect of ORY supplementation was due to modulation of antioxidant defenses avoiding the apoptotic process.
Keyphrases
- liver failure
- oxidative stress
- hepatitis b virus
- cell death
- high fat diet induced
- liver injury
- anti inflammatory
- drug induced
- dna damage
- hydrogen peroxide
- blood pressure
- cell proliferation
- ischemia reperfusion injury
- wild type
- nitric oxide
- single cell
- skeletal muscle
- adipose tissue
- radiation therapy
- acute respiratory distress syndrome