Journal
JOURNAL OF FOOD SCIENCE
Volume 81, Issue 1, Pages H240-H245Publisher
WILEY
DOI: 10.1111/1750-3841.13157
Keywords
Akt; hepatic stellate cell; NF-kappa B; PI3K; resveratrol
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Funding
- National Natural Science Foundation of China [81260664, 813600658]
- Science and Technology Planning Project of Jilin Province for Youth [20150520145JH]
- Tenth Five-Year Plan Science and Technology Planning Project of the Jilin Provincial Education Dept.
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In the present study, we investigated whether resveratrol could suppress the hepatic fibrogenesis in activated hepatic stellate cells. The immortalized rat hepatic stellate cells, t-HSC/Cl-6, were treated with resveratrol 1 h prior to lipopolysaccharide (LPS, 1 mu g/mL). Resveratrol decreased t-HSC/Cl-6 cell viability at much lower concentrations within 24 h. Resveratrol pretreatment also decreased the LPS-induced protein expression of alpha-SMA and collagen I. In addition, resveratrol significantly reduced the protein expression of Toll-like receptor 4 (TLR4) and myeloid differentiation primary response gene 88 (MyD88), and the expression of phosphorylated phosphatidylinositol 3-kinase (PI3K) and phosphorylated serine/threonine kinase B (Akt). Moreover, resveratrol markedly blocked the translocation of nuclear factor (NF)-kappa B in LPS-activated HSCs. Furthermore, resveratrol inhibited HSCs activation through stimulating LXR beta, but did not influence LXR alpha. Overall, we conclude that the antifibrotic effect of resveratrol is the result of blocking NF-kappa B activation and PI3K/Akt phosphorylation, which inhibits HSC activation to obstruct liver fibrosis. Thus, resveratrol may be a natural agent for preventing hepatic fibrosis.
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