{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T05:05:43Z","timestamp":1767848743285,"version":"3.49.0"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":89,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:sec><jats:title>Background and purpose:<\/jats:title><jats:p>Reactive oxygen species (ROC) are the main causes of carbon tetrachloride (CCl<jats:sub>4<\/jats:sub>)\u2010induced acute liver injury. Chondroitin\u20104\u2010sulphate (C4S) is known to inhibit lipid peroxidation through antioxidant mechanisms. Activation of nuclear factor (NF)\u2010\u03baB and caspases may strongly intensify inflammation and cell damage, in addition to that directly exerted by ROS. We investigated whether treatment with C4S, besides exerting antioxidant activity, was able to modulate NF\u2010\u03baB and apoptosis activation in CCl<jats:sub>4<\/jats:sub>\u2010induced liver injury in mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental approach:<\/jats:title><jats:p>Acute hepatitis was induced in mice by an i.p. injection of CCl<jats:sub>4<\/jats:sub>. Varying doses of C4S were administered i.p. 1\u2003h before, 6 and 12\u2003h after CCl<jats:sub>4<\/jats:sub> injection. 24\u2003h after CCl<jats:sub>4<\/jats:sub> injection, the mice were killed for biochemical and histological analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key results:<\/jats:title><jats:p>CCl<jats:sub>4<\/jats:sub> injection produced: marked elevation of alanine aminotransferase and aspartate aminotransferase; hepatic membrane lipid peroxidation, assayed by 8\u2010isoprostane levels; and depletion of reduced glutathione and superoxide dismutase. CCl<jats:sub>4<\/jats:sub> also decreased NF\u2010\u03baB translocation and IkB\u03b1, and increased gene expression of mRNA and protein of metalloproteases (MMP)\u20102 and \u20109, and of pro\u2010 and cleaved forms of caspases\u20103 and \u20107. There was also increased liver polymorphonuclear infiltration, evaluated by elastase assay, and hepatic cell disruption.<\/jats:p><jats:p>C4S treatment inhibited lipid peroxidation; blocked NF\u2010\u03baB activation and IkB\u03b1 protein loss; decreased mRNA and proteins for MMPs and caspases; restored endogenous antioxidants; limited hepatic polymorphonuclear accumulation and tissue damage.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and implications:<\/jats:title><jats:p>As antioxidants may inhibit NF\u2010\u03baB and caspase activation, we hypothesize that treatment with C4S was able to inhibit NF\u2010\u03baB and apoptosis activation in hepatic injury.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2008) <jats:bold>155<\/jats:bold>, 945\u2013956; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/bjp.2008.338\">10.1038\/bjp.2008.338<\/jats:ext-link>; published online 25 August 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