PROTECTION OF METHYLFLAVONOLAMINE AGAINST ACUTE CEREBRAL-ISCHEMIA REPERFUSION INJURY IN RATS

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 su bsequent 1-h release. MFA, 20 mg kg(-1), was injected intravenously 5 min before occlusion and again before release. RESULTS: The brain wate r 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 dism utase (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 p rotein vs Rep, P<0.01) in brain. CONCLUSION: MFA has the protective ef fects on cerebral ischemia/reperfusion, and these effects are relative to scavenging free radicals and anti-lipid peroxidation.