Silybum marianum oil attenuates hepatic steatosis and oxidative stress in high fat diet-fed mice.

In the present study, the effects of Silybum marianum oil (SMO) on hepatic steatosis and oxidative stress were investigated during the development of nonalcoholic fatty liver disease (NAFLD) in high fat diet (HFD)-fed mice. The results showed that body weight, fat mass, and serum biochemical parameters such as triglyceride, free fatty acid, glucose and insulin were reduced by SMO treatment. Meanwhile, SMO decreased the histological injury of liver and the levels of hepatic triglyceride, cholesterol and free fatty acid in HFD-fed mice. SMO administration elevated the activities of superoxide dismutase (SOD) and catalase (CAT) and reduced the level of malondialdehyde (MDA) in the liver. Enzyme linked immunosorbent assay showed that SMO significantly decreased the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in HFD mice. Furthermore, the mRNA levels of sterol regulatory element binding protein 1c (SREBP-1c), fatty acid synthase (FAS) and liver X receptor α (LXRα) were lower, but peroxisome proliferator-activated receptor α (PPARα) was higher in mice treated with SMO compared with the HFD group. The results indicated that SMO could play a certain protective role against HFD-induced NAFLD, and the protective effects might be associated with attenuating lipid accumulation, oxidative stress and inflammation, improving lipid metabolism.

Antioxidant and Anti-aging Activities of Silybum Marianum Protein Hydrolysate in Mice Treated with D-galactose.

OBJECTIVE: In the present study, we investigated the antioxidant and anti-aging effects of Silybum marianum protein hydrolysate (SMPH) in D-galactose-treated mice. METHODS: D-galactose (500 mg/kg body weight) was intraperitoneally injected daily for 7 weeks to accelerate aging, and SMPH (400, 800, 1,200 mg/kg body weight, respectively) was simultaneously administered orally. The antioxidant and anti-aging effects of SMPH in the liver and brain were measured by biochemical assays. Transmission electron microscopy (TEM) was performed to study the ultrastructure of liver mitochondri. RESULTS: SMPH decreased triglyceride and cholesterol levels in the D-galactose-treated mice. It significantly elevated the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC), which were suppressed by D-galactose. Monoamine oxidase (MAO) and malondialdehyde (MDA) levels as well as the concentrations of caspase-3 and 8-OHdG in the liver and brain were significantly reduced by SMPH. Moreover, it increased Bcl-2 levels in the liver and brain. Furthermore, SMPH significantly attenuated D-galactose-induced liver mitochondrial dysfunction by improving the activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase as well as mitochondrial membrane potential (ΔΨm) and fluidity. TEM showed that the degree of liver mitochondrial damage was significantly decreased by SMPH. CONCLUSION: The results indicated that SMPH protects against D-galactose-induced accelerated aging in mice through its antioxidant and anti-aging activities.

Silybum marianum oil attenuates oxidative stress and ameliorates mitochondrial dysfunction in mice treated with D-galactose.

BACKGROUND: Silybum marianum has been used as herbal medicine for the treatment of liver disease, liver cirrhosis, and to prevent liver cancer in Europe and Asia since ancient times. Silybum marianum oil (SMO), a by-product of silymarin production, is rich in essential fatty acids, phospholipids, sterols, and vitamin E. However, it has not been very good development and use. OBJECTIVE: In the present study, we used olive oil as a control to investigate the antioxidant and anti-aging effect of SMO in D-galactose (D-gal)-induced aging mice. MATERIALS AND METHODS: D-gal was injected intraperitoneally (500 mg/kg body weight daily) for 7 weeks while SMO was simultaneously administered orally. The triglycerides (TRIG) and cholesterol (CHOL) levels were estimated in the serum. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), monoamine oxidase (MAO), malondialdehyde (MDA), caspase-3, and Bcl-2 were determined in the liver and brain. The activities of Na(+)-K(+)-adenosine triphosphatase (ATPase), Ca(2+)-Mg(2+)-ATPase, membrane potential (ΔΨm), and membrane fluidity of the liver mitochondrial were estimated. RESULTS: SMO decreased levels of TRIG and CHOL in aging mice. SMO administration elevated the activities of SOD, GSH-Px, and T-AOC, which are suppressed by aging. The levels of MAO and MDA in the liver and brain were reduced by SMO administration in aging mice. Enzyme linked immunosorbent assay showed that SMO significantly decreased the concentration of caspase-3 and improved the activity of Bcl-2 in the liver and brain of aging mice. Furthermore, SMO significantly attenuated the D-gal induced liver mitochondrial dysfunction by improving the activities of Na(+)-K(+)-ATPase, Ca(2+)-Mg(2+)-ATPase, membrane potential (ΔΨm), and membrane fluidity. CONCLUSION: These results indicate that SMO effectively attenuated oxidative damage and improved apoptosis related factors as well as liver mitochondrial dysfunction in aging mice.

Mussel oligopeptides protect human fibroblasts from hydrogen peroxide (H2O2)-induced premature senescence.

Mussel bioactive peptides have been viewed as mediators to maximize the high quality of life. In this study, the anti-aging activities of mussel oligopeptides were evaluated using H2O2-induced prematurely senescent MRC-5 fibroblasts. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry displayed that exposure to H2O2 led to the loss of cell viability and cell cycle arrest. In addition, H2O2 caused the elevation of senescence-associated-ß-galactosidase (SA-ß-gal) activity and formation of senescence-associated heterochromatin foci (SAHF). It was found that pretreatment with mussel oligopeptides could significantly attenuate these properties associated with cellular senescence. Mussel oligopeptides also led to the increase of glutathione (GSH) level and mitochondrial transmembrane potential (Δψm) recovery. In addition, mussel oligopeptides resulted in an improvement in transcriptional activity of peroxiredoxin 1 (Prx1), nicotinamide phosphoribosyltransferase (NAMPT) and sirtuin 1 (SIRT1). This study revealed that mussel oligopeptides could protect against cellular senescence induced by H2O2, and the effects were closely associated with redox cycle modulating and potentiating the SIRT1 pathway. These findings provide new insights into the beneficial role of mussel bioactive peptides on retarding senescence process.