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Effects of scutellarin on liver function after brain ischemia/reperfusion in rats.
Acta Pharmacologica Sinica 2003 November
AIM: To investigate the effects of scutellarin (Scu) on liver function after brain ischemia/reperfusion in Wistar rats.
METHODS: Rats were pretreated with Scu for 7 d and then subjected to a brain ischemia/reperfusion injury induced by a middle cerebral artery occlusion. The levels of nitric oxide (NO), xanthine oxidase (XOD), alanine transaminase (ALT), and aspartate aminotransferase (AST) in serum or liver tissues and the activities of antioxidant enzymes and cytochrome P450-dependent monooxygenases (CYPs) in liver tissues after brain ischemia/reperfusion were determined.
RESULTS: In vehicle-treated rats, XOD, ALT, and AST activities (P<0.01) in serum and the MDA level (P<0.05) in liver tissues were all elevated but were significantly reduced (P<0.05) by Scu pretreatment. The NO levels in serum and liver tissues were decreased (P<0.01) dramatically in vehicle-treated rats and returned to the levels in the sham-operated animals when pretreated with Scu. SOD (P<0.05) and GSH-PX (P<0.01) activities in cytosol fraction were increased significantly by Scu pretreatment. Furthermore, a loss of CYP3A activity (P<0.01), but no changes of CYP1A1, CYP1A2, and CYP2E1 activities in liver were observed after brain ischemia/reperfusion in rats. Scu had no effect on them.
CONCLUSION: These results demonstrated that pretreatment with Scu could attenuate hepatocellular damage elicited by brain ischemia/reperfusion in rats and this protection is in major part by its antioxidant activity.
METHODS: Rats were pretreated with Scu for 7 d and then subjected to a brain ischemia/reperfusion injury induced by a middle cerebral artery occlusion. The levels of nitric oxide (NO), xanthine oxidase (XOD), alanine transaminase (ALT), and aspartate aminotransferase (AST) in serum or liver tissues and the activities of antioxidant enzymes and cytochrome P450-dependent monooxygenases (CYPs) in liver tissues after brain ischemia/reperfusion were determined.
RESULTS: In vehicle-treated rats, XOD, ALT, and AST activities (P<0.01) in serum and the MDA level (P<0.05) in liver tissues were all elevated but were significantly reduced (P<0.05) by Scu pretreatment. The NO levels in serum and liver tissues were decreased (P<0.01) dramatically in vehicle-treated rats and returned to the levels in the sham-operated animals when pretreated with Scu. SOD (P<0.05) and GSH-PX (P<0.01) activities in cytosol fraction were increased significantly by Scu pretreatment. Furthermore, a loss of CYP3A activity (P<0.01), but no changes of CYP1A1, CYP1A2, and CYP2E1 activities in liver were observed after brain ischemia/reperfusion in rats. Scu had no effect on them.
CONCLUSION: These results demonstrated that pretreatment with Scu could attenuate hepatocellular damage elicited by brain ischemia/reperfusion in rats and this protection is in major part by its antioxidant activity.
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