Protection of methylflavonolamine against acute cerebral ischemia reperfusion injury in rats
Abstract
AIM: To examine the possible beneficial action of methylflavonolamine (MFA) on cerebral ischemia/reperfusion injury.
METHODS: Acute cerebral ischemia-reperfusion injury was produced by 4-vessel occlusion and subsequent 1-h release. MFA, 20 mg kg-1, was injected intravenously 5 min before occlusion and again before release.
RESULTS: The brain water content in the reperfusion group (Rep) was elevated (82.7% +/- 1.1% vs control 79.7% +/- 0.5%, P < 0.01), while MFA alleviated the brain edema (80.9% +/- 0.9% vs Rep, P < 0.01). The CK level of brain tissue in Rep decreased (4.7 +/- 1.4 vs control 8.4 +/- 1.2 U/mg protein, P < 0.01), but MFA restored it (7.2 +/- 1.1 U/mg protein vs Rep, P < 0.01). Reperfusion caused the rise of lipid peroxides (2.3 +/- 0.5 vs control 1.5 +/- 0.4 nmol/mg protein, P < 0.01) and weakened the superoxide dismutase (SOD) (3.1 +/- 1.6 vs control 10.5 +/- 3.9 U/mg protein P < 0.01), MFA reduced the rise of lipid peroxides (1.6 +/- 0.4 nmol/mg protein vs Rep, P < 0.05) and protected the activity of SOD (7.9 +/- 1.6 U/mg protein vs Rep, P < 0.01) in brain.
CONCLUSION: MFA has the protective effects on cerebral ischemia/reperfusion, and these effects are relative to scavenging free radicals and anti-lipid peroxidation.
Keywords:
METHODS: Acute cerebral ischemia-reperfusion injury was produced by 4-vessel occlusion and subsequent 1-h release. MFA, 20 mg kg-1, was injected intravenously 5 min before occlusion and again before release.
RESULTS: The brain water content in the reperfusion group (Rep) was elevated (82.7% +/- 1.1% vs control 79.7% +/- 0.5%, P < 0.01), while MFA alleviated the brain edema (80.9% +/- 0.9% vs Rep, P < 0.01). The CK level of brain tissue in Rep decreased (4.7 +/- 1.4 vs control 8.4 +/- 1.2 U/mg protein, P < 0.01), but MFA restored it (7.2 +/- 1.1 U/mg protein vs Rep, P < 0.01). Reperfusion caused the rise of lipid peroxides (2.3 +/- 0.5 vs control 1.5 +/- 0.4 nmol/mg protein, P < 0.01) and weakened the superoxide dismutase (SOD) (3.1 +/- 1.6 vs control 10.5 +/- 3.9 U/mg protein P < 0.01), MFA reduced the rise of lipid peroxides (1.6 +/- 0.4 nmol/mg protein vs Rep, P < 0.05) and protected the activity of SOD (7.9 +/- 1.6 U/mg protein vs Rep, P < 0.01) in brain.
CONCLUSION: MFA has the protective effects on cerebral ischemia/reperfusion, and these effects are relative to scavenging free radicals and anti-lipid peroxidation.