KaeMpferol-3-O-rutinoside, Nicotiflorin;3,4′,5,7-Tetrahydroxyflavone 3-rhamnoglucoside;KaeMpferol-3-O-rutinosid, froM CarthaMus tinctorius;KAEMPFEROL-3-O-RUTINOSIDE;Kaempfeol-3-O-rutinoside;KAEMPFEROL-3-O-RUTINOSIDE WITH HPLC;KAEMPFEROL-3-RUTINOSIDE hplc;3-[[6-O-(6-Deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl]oxy]-2-(4-hydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one
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.
体外研究
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.