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<p> Liver injury induced by CCl<sub>4</sub> is commonly used as model for the screening of hepatoprotective drugs (Janbaz et al., 1995). Liver dysfunction begins soon after injection of CCl<sub>4</sub> and maximum malfunction occurs within 48-72 hr. Induction of CCl<sub>4</sub> eventually leads to hepatocellular necrosis and is reflected in our experiment by marked change in various enzymatic and non-enzymatic parameters of CCl<sub>4 </sub>treated mice and rats. The most serious delayed toxic effects of CCl<sub>4</sub> results from its hepatotoxic and nephrotoxic action (Deichmann and Gerade, 1969). </p> <p> Raised action of serum transaminases (Slater, 1984) in CCl<sub>4</sub>-intoxicated animals is reported to be due to the damaged structural integrity of the liver because these are cytoplasmic in location and are released into circulation after cellular damage (Sallie et al., 1991). In the present study, many fold increase of enzyme leakage as demonstrated by an increased level of serum enzymes ALT, AST, ALP & TB have been noted indicating liver cell damage by CCl<sub>4 </sub>(Tesehke et al., 1983). Use of different extracts of O<em>roxylum indicum</em> prevented leakage of these enzymes and restored the activity of enzymatic variables. </p> <p> Further, significant increase in hepatic LPO and decreased level of SOD, CAT and reduced GSH were observed after CCl<sub>4</sub> exposure. CCl<sub>4</sub> toxicity requires cleavage of the carbon-chloride bond and cleavage takes place after binding of CCl<sub>4</sub> to cytochrome P-450 apoprotein in the mixed function system located in the hepatocellular endoplasmic reticulum (Recknagel and Glande, 1973). CCl<sub>4</sub> is metabolized into trichloromethyl radical (CCl<sub>3</sub>°), which further reacts with molecular oxygen, resulting in the formation of trichloromethyl peroxy radical (CCl<sub>3</sub>O<sub>2</sub>°). Trichloromethyl radical and trichloromehtyl peroxy radical combine with cellular lipid and protein to induce lipid peroxidation by hydrogen abstraction (Kadhska et al., 2000; Lim et al., 2000). </p> <p> Free radical induced oxidative stress has been implicated in disorders, resulting from deficient antioxidant defences. Potential hepatoprotective agents therefore, include either free radical scavenging property or agents, which are capable of augmenting the activity of antioxidant enzymes (Bhattacharya et al., 1997). In the present study, increased malondialdehyde content of liver indicated enhanced lipid peroxidation due to tissue injury in CCl<sub>4</sub> treated control animals. Significant restoration of LPO was observed in animals pretreated with alcoholic, petroleum ether, and n-butanol fraction of root bark of <em>Oroxylum indicum</em> to mice and rats as compared to CCl<sub>4 </sub>control. Pretreatment with extracts of <em>Oroxylum indicum </em>also restored the depleted SOD and CAT levels, demonstrating that the root bark supports the antioxidant defense mechanisms by increasing the activity of enzymes like SOD and CAT. </p> <p> There is a direct co-relation between the enhanced SOD and CAT levels and reduced LPO levels and vice-versa (Gyamfi et al., 1999). In states of oxidative stress, reduced glutathione (GSH) is converted to oxidize glutathione (GSSG) and depletion in it leads to lipid peroxidation. Therefore, the role of GSH as a reasonable marker for evaluation of oxidative stress is important as it acts as an antioxidant, both extracellularly and intracellularly and is produced in the liver (Recknagel et al., 1982). Alcoholic, petroleum ether and n-butanol fractions of root bark of <em>Oroxylum indicum</em> inhibited lipid peroxidation significantly and recovered the decreased hepatic GSH level induced by CCl<sub>4</sub> towards normal. Generation of malondialdehyde like substances were inhibited and delayed by the presence of different extracts of the root bark of <em>Oroxylum indicum </em>during initiation and propagation phases of lipid peroxidation in serum (Sharma et al., 1994). </p> Phytochemical analysis of the root bark of <em>Oroxylum indicum</em> has previously revealed the presence of alkaloids, flavonoids, tannins, and anthraquinones. In the present study, it is suggested that root bark of <em>Oroxylum indicum </em>possesses significant hepatoprotective activity. The mechanism of this activity can be attributed to its antioxidant enzyme activity. It is reported that, flavonoids are known to be antioxidants, free radical scavengers and antilipoperoxidants leading to hepatoprotection. Baicalein, one of the flavonoid is reported to be present in the stem bark of <em>Oroxylum indicum. </em>Baicalein has been shown to possess hepatoprotective activity (Niedworok et al., 1999). HPLC of our earlier study (Data not presented here) has confirmed the presence of baicalein in our plant (Khandhar <em>et. al.,</em> 2006 and Zaveri <em>et. al.,</em> 2008). Therefore, this hepatoprotective activity of our plant might be attributed to the presence of baicalein in <em>O. indicum </em>root bark.
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