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Reversible Hepatic Toxic Effect of Crocin Dyes in Rats
Jen-Kun Lin,Chau-Jong Wang 한국생약학회 1985 생약학회지 Vol.16 No.4
Gardenia jasminodes has been medically used for anti-inflammation, sedation and anti-diarrhea; The extract of this plant has been traditionally used as food colorant and referred as crocin dyes. In the present study, the possible hepatic toxicity of this dye has been evaluted on the basis of its alteration on the marker enzymes, namely, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, alkaline phosphatase, lactate dehydrogenase and gamma-glutamyltransferase. Crocin dyes did not affect hepatic function when they were orally administered to rats in a daily dose of 50 ㎎/㎏ for 8 days, but could induce acute hepatic discoloration. A high dose of 100 ㎎/㎏ for 2 weeks could induce both hepatic damage and black pigmentation, but a lower dose of 10 ㎎/㎏ for 40 days did not The induced black pigmentation and the acute hepatic damage were completely reversible. In conclusion, the crocin dyes have a very low hepatic toxicity in rats, even in high experimental dosages which could hardly happen in human practice. It is therefore suggested that the crocin dyes are safe for coloring foods.
Chi-Nan Hung,Hui-Pei Huang,Chau-Jong Wang,Kai-Li Liu,Chong-Kuei Lii 한국식품영양과학회 2014 Journal of medicinal food Vol.17 No.10
Endothelial dysfunction is an early indicator of cardiovascular diseases. Increased stimulation of tumor necrosis factor-a (TNF-a) triggers the inflammatory mediator secretion of endothelial cells, leading to atherosclerotic risk. In this study, we investigated whether sulforaphane (SFN) affected the expression of intracellular adhesion molecule-1 (ICAM-1) in TNF-a-induced ECV 304 endothelial cells. Our data showed that SFN attenuated TNF-a-induced expression of ICAM-1 in ECV 304 cells. Pretreatment of ECV 304 cells with SFN inhibited dose-dependently the secretion of proinflammatory cytokines, such as interleukin (IL)-1b, IL-6, and IL-8. SFN inhibited TNF-a-induced nuclear factor-jB (NF-jB) DNA binding activity. Furthermore, SFN decreased TNF-a-mediated phosphorylation of IjB kinase (IKK) and IjBa, Rho A, ROCK, ERK1/2, and plasminogen activator inhibitor-1 (PAI-1) levels. Collectively, SFN inhibited the NF-jB DNA binding activity and downregulated the TNF-a-mediated induction of ICAM-1 in endothelial cells by inhibiting the Rho A/ROCK/NF-jB signaling pathway, suggesting the beneficial effects of SFN on suppression of inflammation within the atherosclerotic lesion.