Name | kaempferol-3-rutinoside |
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Synonyms |
kaempferol-3-O-rutinoside
Nicotiflorin Kaempferol 3-O-rutinose 5,7-dihydroxy-2-(4-hydroxyphenyl)-3-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxymethyl]oxan-2-yl]oxychromen-4-one 4H-1-Benzopyran-4-one, 3-[[6-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl]oxy]-5,7-dihydroxy-2-(4-hydroxyphenyl)- 5,7-Dihydroxy-2-(4-hydroxyphenyl)-4-oxo-4H-chromen-3-yl 6-O-(6-deoxy-a-L-mannopyranosyl)-b-D-glucopyranoside 5,7-Dihydroxy-2-(4-hydroxyphenyl)-4-oxo-4H-chromen-3-yl 6-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranoside Nicotiflorine 4H-1-Benzopyran-4-one, 3-((6-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl)oxy)-5,7-dihydroxy-2-(4-hydroxyphenyl)- kaempferol 3-O-rutinoside NICOTIFLOROSIDE Kaempferol 3-O-β-rutinoside Kaempferol-3-rutinoside kaempferol-3-rhamnoglucoside |
Description | Nicotiflorin is a flavonoid glycoside extracted from a traditional Chinese medicine Flos Carthami. Nicotiflorin shows potent antiglycation activity and neuroprotection effects. |
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Related Catalog | |
Target |
Antiglycation[1] |
In Vitro | 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[2]. 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[3]. |
In Vivo | 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[2]. Nicotiflorin (2.5-10 mg/kg) administered after onset of ischemia markedly reduces brain infarct volume by 24.5-63.2% and neurological deficits[3]. |
Cell Assay | Cortical neurons are treated with nicotiflorin (25-100 mg/mL) just before hypoxia. Cell viability is determined using the MTT assay[2]. |
Animal Admin | Rats[2] A neurological examination is performed on each rat 24 h after the onset of ischemia. Briefly, neurological scores (NS) are derived using a 10-point sliding scale. Rats are administered 2.5, 5, and 10 mg/kg nicotiflorin or vehicle immediately after occlusion. Each animal is examined for reduced resistance to lateral push (score, 4), open field circling (score, 3), and shoulder adduction (score, 2) or contralateral forelimb flexion (score, 1) when held by the tail and suspended approximately 0.5 m above the floor. Rats extending both forelimbs toward the floor and not showing any other signs of neurological impairment are scored 0[2]. |
References |
Density | 1.76 |
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Boiling Point | 941.7±65.0 °C at 760 mmHg |
Melting Point | 181-186 ºC |
Molecular Formula | C27H30O15 |
Molecular Weight | 594.518 |
Flash Point | 312.8±27.8 °C |
Exact Mass | 594.158447 |
PSA | 249.20000 |
LogP | 1.96 |
Vapour Pressure | 0.0±0.3 mmHg at 25°C |
Index of Refraction | 1.744 |
Storage condition | ?20°C |