Antihyperlipidemic effect of Acanthopanax senticosus (Rupr. et Maxim) Harms leaves in high-fat-diet fed mice.

BACKGROUND: Metabolic syndrome is a major risk factor for a variety of obesity-related diseases. Recently, the effects of functional foods have been investigated on lipid metabolism as a means to reduce lipid content in the blood, liver and adipose tissues associated with carnitine O-palmitoyltransferase (CPT) activity. Acanthopanax senticosus (Rupr. et Maxim) Harms (AS) is a medicinal herb possessing a wide spectra of functions including antioxidant, anti-inflammatory and anti-fatigue actions. Despite much research being focused on the cortical roots of AS, little information is available regarding its leaves, which are also expected to promote human health, for example by improving abnormal lipid metabolism. Here, we explored whether AS leaves affect lipid metabolism in mice fed a high-fat diet. RESULTS: The administration of AS to BALB/c mice fed a high-fat diet significantly decreased plasma triglycerides (TG). CPT activity in the liver of these mice was significantly enhanced by AS treatment. CONCLUSION: These findings indicate that AS leaves have the potential to alleviate increase in plasma TG levels due to high-fat diet intake in mice, possibly by increasing mitochondrial fatty acid ß-oxidation, especially via CPT activation. Consequently, daily intake of AS leaves could promote beneficial health effects including the prevention of metabolic syndrome. © 2015 Society of Chemical Industry.

Metabolic Fate of Luteolin in Rats: Its Relationship to Anti-inflammatory Effect.

Luteolin is a naturally occurring flavone that reportedly has anti-inflammatory effects. Because most luteolin is conjugated following intestinal absorption, free luteolin is likely present at low levels in the body. Therefore, luteolin metabolites are presumably responsible for luteolin bioactivity. Here we confirmed that luteolin glucuronides, especially luteolin-3'-O-glucuronide, are the major metabolites found in plasma after oral administration of luteolin (aglycone) or luteolin glucoside (luteolin-7-O-glucoside) to rats. Luteolin-4'-O-glucuronide and luteolin-7-O-glucuronide were also detectable together with luteolin-3'-O-glucuronide in the liver, kidney, and small intestine. Next, we prepared these luteolin glucuronides and compared the anti-inflammatory effects of luteolin and luteolin glucuronides on gene expression in lipopolysaccharide-treated RAW264.7 cells. Luteolin glucuronides, especially luteolin-7-O-glucuronide, reduced expression of inflammatory genes in the cells, although their effects were weaker than those of luteolin. These results indicate that the active compound responsible for the anti-inflammatory effect of luteolin in vivo would be luteolin glucuronide and/or residual luteolin.

Ingestion of Chlorella reduced the oxidation of erythrocyte membrane lipids in senior Japanese subjects.

Accumulation of phospholipid hydroperoxide (PLOOH) in erythrocyte membranes is an abnormality found in patients with senile dementia, including those with Alzheimer's disease. In our previous studies, dietary xanthophylls (polar carotenoids such as lutein) were hypothesized to inhibit lipid peroxidation. In the present study, we conducted a randomized, double-blind, placebo-controlled human trial to assess the impact for a total of 2 months Chlorella supplementation (8 g Chlorella/day/person; equivalent to 22.9 mg lutein/day/person) on PLOOH and carotenoid concentrations in erythrocytes as well as plasma of 12 normal senior subjects. After 1 or 2 months of treatment, erythrocytes and plasma lutein concentrations increased in the Chlorella group but not in the placebo group. In the Chlorella-supplemented group, erythrocyte PLOOH concentrations after a total of 2 months of treatment were lower than the concentrations before supplementation. These results suggest that Chlorella ingestion improved erythrocyte antioxidant status and lowered PLOOH concentrations. These reductions might contribute to maintaining the normal function of erythrocytes and prevent the development of senile dementia.