Improved Hepatoprotective Effect of Liposome-Encapsulated Astaxanthin in Lipopolysaccharide-Induced Acute Hepatotoxicity

• Published in: International journal of molecular sciences Vol. 17; no. 7; p. 1128
• Main Authors: Chiu, Chun-Hung, Chang, Chun-Chao, Lin, Shiang-Ting, Chyau, Charng-Cherng, Peng, Robert Y
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 14.07.2016; MDPI
• Subjects: Animals; antioxidant enzymes; Antioxidants; Antioxidants - metabolism; Astaxanthin; Body Weight - drug effects; Chemical and Drug Induced Liver Injury - etiology; Chemical and Drug Induced Liver Injury - metabolism; Chemical and Drug Induced Liver Injury - prevention & control; Fibrinolytic Agents - pharmacology; Glutathione - metabolism; Hepatology; hepatotoxicity; inflammation; Interleukin-6 - metabolism; Lipopolysaccharides - toxicity; liposome encapsulation; Liposomes - administration & dosage; Liposomes - chemistry; Male; Malondialdehyde - metabolism; Nanocapsules - administration & dosage; Nanocapsules - chemistry; NF-kappa B - metabolism; Nitric Oxide Synthase Type II - metabolism; Organ Size - drug effects; Oxidative Stress; Protective Agents - pharmacology; Rats; Rats, Sprague-Dawley; Toxicity; Xanthophylls - pharmacology; antioxidant enzymes; liposome encapsulation; inflammation; Astaxanthin; hepatotoxicity
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms17071128

Lipopolysaccharide (LPS)-induced acute hepatotoxicity is significantly associated with oxidative stress. Astaxanthin (AST), a xanthophyll carotenoid, is well known for its potent antioxidant capacity. However, its drawbacks of poor aqueous solubility and low bioavailability have limited its utility. Liposome encapsulation is considered as an effective alternative use for the improvement of bioavailability of the hydrophobic compound. We hypothesized that AST encapsulated within liposomes (LA) apparently shows improved stability and transportability compared to that of free AST. To investigate whether LA administration can efficiently prevent the LPS-induced acute hepatotoxicity, male Sprague-Dawley rats (n = six per group) were orally administered liposome-encapsulated AST at 2, 5 or 10 mg/kg-day (LA-2, LA-5, and LA-10) for seven days and then were LPS-challenged (i.p., 5 mg/kg). The LA-10 administered group, but not the other groups, exhibited a significant amelioration of serum glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), blood urea nitrogen (BUN), creatinine (CRE), hepatic malondialdehyde (MDA) and glutathione peroxidase (GSH-Px), IL-6, and hepatic nuclear NF-κB and inducible nitric oxide synthase (iNOS), suggesting that LA at a 10 mg/kg-day dosage renders hepatoprotective effects. Moreover, the protective effects were even superior to that of positive control N-acetylcysteine (NAC, 200 mg/kg-day). Histopathologically, NAC, free AST, LA-2 and LA-5 partially, but LA-10 completely, alleviated the acute inflammatory status. These results indicate that hydrophobic AST after being properly encapsulated by liposomes improves bioavailability and can also function as potential drug delivery system in treating hepatotoxicity.