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Publication : Pycnogenol protects against diet-induced hepatic steatosis in apolipoprotein-E-deficient mice.

First Author  Wang D Year  2018
Journal  Am J Physiol Endocrinol Metab Volume  315
Issue  2 Pages  E218-E228
PubMed ID  29462565 Mgi Jnum  J:270242
Mgi Id  MGI:6204544 Doi  10.1152/ajpendo.00009.2017
Citation  Wang D, et al. (2018) Pycnogenol protects against diet-induced hepatic steatosis in apolipoprotein-E-deficient mice. Am J Physiol Endocrinol Metab 315(2):E218-E228
abstractText  Pycnogenol(R) (PYC), a combination of active flavonoids derived from French maritime pine bark, is a natural antioxidant that has various pharmacological activities. Here, we investigated the beneficial effect of PYC on diet-induced hepatic steatosis. Apolipoprotein E (ApoE)-deficient male mice were administered PYC at oral doses of 30 or 100 mg.kg(-1).day(-1) for 2 wk in advance and were then fed a high-cholesterol and -fat diet (HCD) for 8 wk. Biochemical, immunohistochemical, and gene expression analyses were conducted to explore the effect of PYC on lipid metabolism in ApoE-deficient mice on a HCD. Short-term treatment with HCD in ApoE-deficient mice induced hepatic injuries, such as lipid metabolism disorder and hepatic histopathological changes. We found that PYC reduced body weight and the increase of serum lipids that had been caused by HCD. Supplementation of PYC significantly reduced lipid deposition in the liver, as shown by the lowered hepatic lipid content and histopathological lesions. We subsequently detected genes related to lipid metabolism and inflammatory cytokines. The study showed that PYC markedly suppressed the expression of genes related to hepatic lipogenesis, fatty acid uptake, and lipid storage while increasing the lipolytic gene, which thus reduced hepatic lipid content. Furthermore, PYC mainly reduced the expression of inflammatory cytokines and the infiltration of inflammatory cells, which were resistant to the development of hepatic steatosis. These results demonstrate that PYC protects against the occurrence and development of hepatic steatosis and may provide a new prophylactic approach for nonalcoholic fatty liver disease (NAFLD).
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