The bark of Prunus yedoensis is used in antitussive medicines and in oral herbal formulations for inflammatory skin disorders. In the present study, we explored whether P. yedoensis bark extract (PYE) and its solvent partitioned fractions could modulate lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-a and interleukin (IL)-6 in vivo and in vitro. In addition, we examined the effect of PYE extract and its fractions on LPS-induced NF-jB and mitogen-activated protein kinase (MAPK) signaling in mouse peritoneal macrophages. Oral treatment of PYE decreased serum levels of TNF-a and IL-6 in LPS injected mice. PYE inhibited LPS-induced TNF-a and IL-6 in macrophages at the transcriptional level and also suppressed LPS-induced IjBa degradation and MAPK activation in vitro. Among the fractions, the chloroform fraction, which contains genistein, naringenin, sakuranetin, prunetin, and amygdalin, showed inhibitory effects at much lower concentrations than the water and ethyl acetate fractions. Taken together, our results indicate that PYE was able to inhibit LPS-induced expression of TNF-a and IL-6, the latter of which was more prominent. The effects of PYE on inflammatory cytokine synthesis may involve modulation of NF-jB and MAPK activation.

The present study aimed to investigate the antihypercholesterolemic effects of krill oil supplementation in high-cholesterol diet-induced hypercholesterolemic rats, and the mechanisms underlying these effects. Rats were divided into five groups: normal control, control (high-cholesterol diet), krill oil 100 mg/kg b.w. (high-cholesterol diet with Krill oil 100 mg/kg b.w.), and krill oil 200 mg/kg b.w. (high-cholesterol diet with Krill oil 200 mg/kg b.w.). After 12 weeks, the rats were sacrificed to observe the effects of krill oil on cholesterol synthesis and excretion. We found that krill oil supplementation suppressed total triglycerides, total cholesterol, and LDL-cholesterol levels, as well as HMG-CoA reductase activity. It stimulated AMPK phosphorylation, LDL receptor and ACAT2 expression in the liver, and the fecal output of cholesterol. Furthermore, it decreased the levels of P-selectin, sVCAM-1, and NO, as well as aortic wall thickness, demonstrating its role in the prevention of atherosclerosis. Thus, we suggest that krill oil supplementation can reduce LDL-cholesterol levels in the blood during hypercholesterolemia by stimulating the uptake of LDL-cholesterol into tissue and cholesterol excretion, as well as inhibition of cholesterol synthesis.

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Background: Obesity, abnormal fat accumulation in the adipose tissue, has become a serious global public health problem as it increases an individual’s risk of developing various diseases. Objective: This study sought to determine whether the extract from sunflower seed (SUNCA) prevents the development of obesity in high-fat diet (HFD)-induced obese mice. Design: C57BL/6J mice were fed with AIN93G normal diet (Normal diet), 60% HFD, HFD containing Catechin 100 mg/kg body weight (b.w.) (Catechin), HFD containing SUNCA 25 mg/kg b.w. (SUNCA 25), HFD containing SUNCA 50 mg/kg b.w. (SUNCA 50), or HFD containing SUNCA 100 mg/kg b.w. (SUNCA 100) for 15 weeks. Results: Body weight gain, food efficiency rate, adipose tissue weight, adipose tissue mass, size of adipocytes, and serum levels of triglyceride, total cholesterol, very low-density lipoprotein/low-density lipoprotein (VLDL/LDL)-cholesterol, aspartate aminotransferase, and alanine aminotransferase were significantly decreased by SUNCA supplementation in HFD-fed mice. Furthermore, SUNCA supplementation decreased the expression of proteins related to the adipogenesis and lipogenesis pathways and increased the expression of proteins related to the lipolysis and thermogenesis pathways in the adipose tissues of HFD-induced obese mice. Conclusions: Altogether, SUNCA might prevent obesity by suppressing the adipogenesis/lipogenesis pathway and stimulating the lipolysis/thermogenesis pathway in HFD-induced obese mice.

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