Permanent Focal Cerebral Ischemia And Effects Of Interference With Ginsenoside Rg₂

OBJECTIVE To observe relationship between changes of cerebral blood flow, biochemical metabolism and extent of cerebral damage by permanent focal cerebral ischemia, we studied mechanism of cerebral ischemic injury and effects of ginsenoside Rg2. METHODS The model is established by left middle cerebral artery occlusion (MCAO) for 6 hours via tansorbital approach without reperfusion. MFV-1200 electromagnetic flowmeter was used to record cerebral blood flow (CBF) at 5, 10, 20, 40, 60min., and 2, 4, 6hour after onset of ischemia. Then cats were sacrificed and left hemispheric fresh tissue processed for TTC staining to assess the infarct area from anatomic-graded brain slices (3mm thick). SOD, MDA, and LA in homogenate were measured with biochemical techniques. RESULTS MCAO for 6 hours produced irreversible injury to brain. Preischemic treatment groups with ginsenoside Rg2 i.v. (1, 2, 4 mg/kg ) or Nimodipine i.v. (20ug/kg) reduced infarct area significantly (p<0.01) by 15 + 2%, 27+5%, 38 + 3%, and 30+3% respectively compared with model group. But there was no difference in CBF and other physiological parameters among groups. In ischemic temporoparietal cortex, activity of SOD decreased and content of MDA increased. Ginsenoside Rg2 and Nimodipine can markedly ameliorated the decreased activity of SOD and preserved the amount of MAD close to that in sham-operation cats. Lactic acidosis secondary to MCAO was attenuated for pretreatment of ginsenoside Rg2 rather than nimodipine. CONCLUSION In this experimental model of focal ischemia lacking reperfusion in cats, ginsenoside Rg2 has a neuroprotective potential against ischemic-induced injury which may be partly contributed to improving the antioxydation and the inhibition of metabolic acidosis within lesioned region.Tang lie (physiology)Directed by - Jin Yi...