• Proceedings of the Korean Society of Life Science Conference
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• 2005.04a
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• pp.226-226
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• 2005

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.113.2-113.2
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• 2003

Inducible cyclooxygenase-2 (COX-2) has been implicated in the processes of inflammation and carcinogenesis. Thus, the potential COX-2 inhibitors have been considered as anti-inflammatory or cancer chemopreventive agents. In this study, we investigated the effect of Caffeoyl-4-dihydrocaffeoyl quinic acid (CDCQ) isolated from Salicornia herbacea on the expression of cyclooxygenase (COX-2) in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. When CDCQ was treated with LPS, the prostaglandin $E_2$ production and COX-2 gene expression induced by LPS were markedly reduced in a dose-dependent manner. (omitted)

• Archives of Pharmacal Research
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• v.28 no.10
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• pp.1122-1126
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• 2005

Tungtungmadic acid (3-caffeoyl-4-dihydrocaffeoyl quinic acid) is a new chlorogenic acid derivative that was isolated from the Salicomia herbacea. The structure of tungtungmadic acid was determined using chemical and spectral analysis. The antioxidant activity of tungtungmadic acid was evaluated using various antioxidant assays, including free radical scavenging, lipid peroxidation and hydroxyl radical-induced DNA strand breaks assays. Tungtungmadic acid ($IC_{50}\;=\;5.1\;{\mu}M\;and\;9.3\;{\mu}M$) was found to have higher antioxidant activity in the DPPH scavenging assay as well as in the iron-induced liver microsomal lipid peroxidation system. In addition, the tungtungmadic acid was also effective in protecting the plasmid DNA against strand breakage induced by hydroxyl radicals.

• Toxicological Research
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• v.22 no.3
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• pp.267-273
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• 2006

Tungtungmadic acid(3-caffeoyl, 4-dihydrocaffeoyl quinic acid: CDCQ) is a new chlorogenic acid derivative isolated from the Salicornia herbacea. The suppressive effects of CDCQ on the progress of acute carbon tetrachloride($CCl_4$)-induced hepatic fibrosis were investigated in mice. CDCQ significantly suppressed $CCl_4$-induced hepatic necrosis and inflammation, as determined by serum enzymatic activities of alanine and aspartate aminotransferase and serum TNF-$\alpha$ levels in a dose-dependent manner. In addition, increased hepatic lipid peroxidation and fibrosis after acute $CCl_4$ treatment were suppressed by the administration of CDCQ. CDCQ also significantly prevented the elevation of hepatic hydroxyproline and collagen content and ${\alpha}$-smooth muscle actin(${\alpha}$-SMA) expression in the liver of $CCl_4$-intoxicated mice. These results suggest that the suppressive effects of CDCQ against the acute $CCl_4$-induced hepatic fibrosis possibly related to its ability to block both hepatic inflammation and the activation of hepatic stellate cells.