Abstract
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.
Highlights
Astaxanthin (3,31 -dihydroxy-β,β1 -carotene-4,41 -dione) (AST, Scheme 1) is a xanthophyll carotenoid contained in Haematococcus pluvialis, Chlorella zofingiensis, Chlorococcum, and Phaffia rhodozyma
The supernatant was used for determination of the levels of blood urea nitrogen (BUN), creatinine (CRE), glutamate-pyruvate transaminase (GPT), glutamate-oxaloacetate transaminase (GOT), nitrite, interleukine-6 (IL-6), and tumor necrosis factor-α (TNF-α)
The poor bioavailability of astaxanthin in reality has been improved by the liposome-encapsulation technology
Summary
Astaxanthin (3,31 -dihydroxy-β,β1 -carotene-4,41 -dione) (AST, Scheme 1) is a xanthophyll carotenoid contained in Haematococcus pluvialis, Chlorella zofingiensis, Chlorococcum, and Phaffia rhodozyma. Applications, Regarding biomedical applications, AST is often used as aannutritional supplement, an agent, and a preventive agent against diabetes, cardiovascular diseases, and neurodegenerative antioxidant, an anticancer agent, and a preventive agent against diabetes, cardiovascular diseases, disorders to effectively disorders stimulateto immunity and suppress carcinogenesis due tocarcinogenesis its potent oxygen and neurodegenerative effectively stimulate immunity and suppress due radical-scavenging activity and anti-carcinoma prognosis [1,4,5]. AST, an antioxidant marine carotenoid, restored physiological conditions in U937 cells stimulated with LPS (10 mg/mL) [9]. Our previous study demonstrated that poor bioavailability of AST can be improved by liposomal of AST can be improved by liposomal encapsulation and it represents an effective agent for encapsulation and it represents an effective agent for improving the stability and transportability improving the stability and transportability of AST in hepatic cell lines [15]. These two preparations (FA and LAs) were tested for their against LPS-induced hepatotoxicity.
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