Anti-oxidative and anti-inflammatory effects of lipoic acid in rat liver.
BACKGROUND
Lipopolysaccharide (LPS) is a key inflammatory component of Gram-negative bacteria, which after entering the systemic circulation contributes to the development of septic hepatic failure.


OBJECTIVE
The aim of this study was to evaluate the effects of alpha lipoic acid (LA) on oxidative stress parameters and inflammation in endotoxemic rat liver.


METHODS
Male Wistar rats were divided into 4 groups, each group consisting of 8 animals. Group I received saline and served as a control, Group II received a single dose of LA (60 mg/kg i.v.), Group III received lipopolysaccharide (LPS) (15 mg/kg i.v.), and Group IV received LPS (15 mg/kg i.v.) and 30 min later received LA (60 mg/kg i.v.). Five hours after LPS or LA administration, the animals were sacrificed and the liver was isolated for measurements of levels of thiobarbituric acid reactive substances (TBARS), hydrogen peroxide (H2O2), total sulfhydryl groups (-SH), total glutathione (tGSH) and reduced glutathione (GSH).


RESULTS
Injection of LPS caused a significant increase in liver TBARS and H2O2 levels and a significant decrease in levels of -SH groups, tGSH and GSH. LPS-treated rats also showed an increase in TNF-α and IL-6 levels and edema in the liver. The administration of LA to endotoxemic rats significantly reduced TBARS, H2O2, TNF-α, and IL-6 levels and reduced edema in the liver when compared to the LPS group. This antioxidant also resulted in an increase in -SH groups and tGSH and GSH levels and ameliorated the glutathione redox status when compared to the LPS group.


CONCLUSIONS
The results indicated that LA administered 30 min following LPS infusion may effectively prevent oxidative stress and inflammation in the liver. Thus LA is a potent antioxidant that can be useful in rebuilding LPS-induced damaged liver tissue.
Experimental and Clinical Physiology, Department of Cardiovascular Physiology, Medical University of Lodz, Poland.
Anna
A
Goraca
Experimental and Clinical Physiology, Department of Cardiovascular Physiology, Medical University of Lodz, Poland.
Halina
H
Huk-Kolega
Experimental and Clinical Physiology, Department of Cardiovascular Physiology, Medical University of Lodz, Poland.
Agata
A
Kowalczyk
Department of Applied Pharmacy, Faculty of Pharmacy, Medical University of Lodz, Poland.
Beata
B
Skibska
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D005978:Glutathione / Q000032:analysis; D006861:Hydrogen Peroxide / Q000032:analysis; D007249:Inflammation / Q000188:drug therapy; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008099:Liver / Q000737:chemistry* / Q000187:drug effects*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013438:Sulfhydryl Compounds / Q000032:analysis; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D008063:Thioctic Acid / Q000494:pharmacology*
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D008070:Lipopolysaccharides; D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; D008063:Thioctic Acid; D006861:Hydrogen Peroxide; D005978:Glutathione