山柰酚-3-O-芸香糖苷

For primarily cultured neurons suffered 2 h hypoxia followed by 24 h reoxygenation, nicotiflorin significantly attenuates cell death and reduces LDH release. Morphological observation also directly confirms its protective effect on neuron. After total 4 h hypoxia and 12 h reoxygenation, eNOS activity, mRNA and protein levels in the primarily cultured rat cerebral blood vessel endothelial cells treated with nicotiflorin (25-100 g/mL) 2 h after onset of hypoxia are significantly higher than eNOS activity, mRNA and protein levels in the pure H-R cells and also higher than eNOS activity, mRNA and protein levels in cells cultured under normoxic conditions.

At doses of 2.5, 5 and 10 mg/kg, nicotiflorin administered immediately after the onset of ischemia markedly reduces brain infarct volume and neurological deficits. Nicotiflorin (2.5-10 mg/kg) administered after onset of ischemia markedly reduces brain infarct volume by 24.5-63.2% and neurological deficits.