Guest guest Posted September 2, 2000 Report Share Posted September 2, 2000 http://www.infotrieve.com/healthworld/std_format.cgi?med93-95+593187+(schisandra\ )+AND+(liver) -- Chinese Herbal Medicine Title Schisandrin B protects against carbon tetrachloride toxicity by enhancing the mitochondrial glutathione redox status in mouse liver. Author Ip SP; Poon MK; Che CT; Ng KH; Kong YC; Ko KM Address Department of Biochemistry, Hong Kong University of Science Technology, Hong Kong. Source Free Radic Biol Med, 21(5):709-12 1996 Abstract Previous studies in our laboratory have demonstrated the effect of Schisandrin B (Sch B),an active ingredient of the fruit of Schisandra chinensis, on enhancing the hepatic glutathione antioxidant system in mice, as evidenced by the hepatoprotection against carbon tetrachloride (CCl4) toxicity. In the present study, the mechanism involved in the hepatoprotection afforded by Sch B treatment was investigated. Treating female Balb/c mice with 1, 3-bis(2-chloroethyl)-1-nitrosourea, an inhibitor of glutathione reductase (GRD), at a dose of 2 mmol/kg (i.p.) did not abrogate the hepatoprotective action of Sch B in CCl4-treated mice. The result indicates that the increased activity of hepatic GRD is not ascribable to the hepatoprotective action of Sch B. In control mice, the same Sch B treatment regimen caused an enhancement in hepatic mitochondrial glutathione redox status, as indicated by the significant increase and decrease in reduced and oxidized glutathione levels, respectively. While the CCl4 intoxication greatly impaired mitochondrial glutathione redox status, the beneficial effect of Sch B treatment became more evident after CCl4 challenge. Our results strongly suggest that the mechanism of hepatoprotection afforded by Sch B treatment may involve the enhancement of mitochondrial glutathione redox status. Language Eng Unique Identifier 97046753 MESH Headings Alanine Transaminase BL ; Animal ; Antioxidants *PD ; Carbon Tetrachloride *AI/*TO ; Enzyme Inhibitors PD ; Female ; Free Radicals ME ; Glutathione AA/*ME ; Glutathione Reductase AI ; Mice ; Mice, Inbred BALB C ; Mitochondria, Liver *DE/*ME ; Oxidation-Reduction ; Polycyclic Hydrocarbons *PD ; Support, Non-U.S. Gov't Publication Type JOURNAL ARTICLE ISSN 0891-5849 Country of Publication UNITED STATES Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 2, 2000 Report Share Posted September 2, 2000 leukotrienes ...>>>>Suppression of leukotrienes may explain why it is wu wei zi is effective is heart disease. very interesting. Thanks Todd - cha Friday, September 01, 2000 11:07 PM wu wei zi http://www.infotrieve.com/healthworld/std_format.cgi?med90-92+283090+(schisandra)+AND+(liver)--Todd LugerDirectorChinese Herbal Medicinehttp://www..orgChinese Herbal Medicine, a voluntary organization of licensed healthcare practitioners, matriculated students and postgraduate academics specializing in Chinese Herbal Medicine, provides a variety of professional services, including board approved online continuing education. Title Effect of gomisin A (TJN-101) on the arachidonic acid cascade in macrophages. Author Ohkura Y; Mizoguchi Y; Morisawa S; Takeda S; Aburada M; Hosoya E Address Third Department of Internal Medicine, Osaka City University Medical School, Japan. Source Jpn J Pharmacol, 52(2):331-6 1990 Feb Abstract It has been reported that leukotrienes (LTs) may play a role in inflammatory liver diseases, and several inhibitors of LTs show an inhibitory effect on experimental liver injuries. In this study, the effect of Gomisin A (TJN-101), which is a lignan component of schisandra fruits, on the arachidonic acid cascade in macrophages was examined to explain the mechanisms of the inhibitory effect of TJN-101 on liver injuries. The production of leukotriene B4 was suppressed by treatment with TJN-101, while the activity of 5-lipoxygenase was not affected. The release of arachidonic acid from macrophages stimulated with fMet-Leu-Phe or the Ca++ ionophore A23187 was suppressed by treatment with TJN-101. The activity of phospholipase A2 was not affected by treatment with TJN-101. These results suggested that TJN-101 produces an inhibitory effect on the biosynthesis of LTs by preventing the release of arachidonic acid, and it was thought that the preventive effect on the arachidonic acid cascade may be partially associated with the inhibitory effect of TJN-101 on liver injuries. Language Eng Unique Identifier 90189556 MESH Headings Animal ; Arachidonic Acids *ME ; Exudates and Transudates DE/ME ; Hepatitis, Toxic PC ; Leukotriene B4 BI LEUKOTRIENE B 04 ; Lipoxygenase ME ; Macrophages DE/*ME ; Male ; Phospholipases A AI ; Polycyclic Hydrocarbons *PD/TU ; Rats ; Rats, Inbred Strains Publication Type JOURNAL ARTICLE ISSN 0021-5198 Country of Publication JAPAN Quote Link to comment Share on other sites More sharing options...
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