{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T04:35:14Z","timestamp":1771562114409,"version":"3.50.1"},"reference-count":45,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2008,12,4]],"date-time":"2008-12-04T00:00:00Z","timestamp":1228348800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hepatology Research"],"published-print":{"date-parts":[[2009,3]]},"abstract":"<jats:p><jats:bold>Aim:\u2002<\/jats:bold>The curative effect of emodin (1,3,8\u2010trihydroxy\u20106\u2010methyl anthraquinone), an active compound of the plant species<jats:italic>Ventilago maderaspatana<\/jats:italic>Gaertn, was evaluated against carbon tetrachloride (CCl<jats:sub>4<\/jats:sub>) induced hepatic cytochrome P450 (CYP) enzymatic and ultrastructural alterations in rats.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold>Female rats were administered CCl<jats:sub>4<\/jats:sub>(1.5\u2003mL\/kg, ip) followed by varying doses of emodin (20, 30 and 40\u2003mg\/kg, oral po) after 24\u2003h of CCl<jats:sub>4<\/jats:sub>administration. Animals were euthanized after 24\u2003h of last administration to determine liver function tests in serum, hepatic light microscopic and ultrastructural changes, activity of CYP enzymes, microsomal lipid peroxidation and protein contents, hexobarbitone induced sleep time and bromosulphalein retention.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold>The CCl<jats:sub>4<\/jats:sub>induced\u2010toxic effects were observed with sharp elevation in the release of serum transaminases, alkaline phosphatase, lactate dehydrogenase and \u03b3\u2010glutamyl transpeptidase. An initial study for an optimum dose of emodin among different dose levels revealed that a 30\u2003mg\/kg dose was effective in restoring all the enzymatic variables and liver histoarchitecture in a dose dependent manner. Exposure to CCl<jats:sub>4<\/jats:sub>diminished the activities of CYP enzymes (i.e. aniline hydroxylase and amidopyrine\u2010N\u2010demethylase and microsomal protein contents with concomitant increase in microsomal lipid peroxidation). Emodin at 30\u2003mg\/kg effectively reversed the CCl<jats:sub>4<\/jats:sub>induced hepatotoxic events, which was consistent with ultrastructural observations. Hexobarbitone\u2010induced sleep time and plasma bromosulphalein retention also improved liver functions after emodin therapy.<\/jats:p><jats:p><jats:bold>Conclusion:\u2002<\/jats:bold>By reversal CYP activity and ultrastructural changes, emodin shows a strong hepatoprotective abilities.<\/jats:p>","DOI":"10.1111\/j.1872-034x.2008.00380.x","type":"journal-article","created":{"date-parts":[[2008,12,4]],"date-time":"2008-12-04T14:10:13Z","timestamp":1228399813000},"page":"290-300","source":"Crossref","is-referenced-by-count":23,"title":["Emodin reverses CCl<sub>4<\/sub>induced hepatic cytochrome P450 (CYP) enzymatic and ultrastructural changes: The<i>in vivo<\/i>evidence"],"prefix":"10.1111","volume":"39","author":[{"given":"Monika","family":"Bhadauria","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Satendra 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