prld2gr8ns
Idiot Savant
Thought this was an interesting find about Quercitrin and it's role as an anti-inflammatory agent in the intestines.
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Glycosidic form of quercetin helps protect against IBD induced conditions
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prld2gr8ns
Idiot Savant
Here's another short write-up talking about it's role in lipid oxidation levels by measurement of the oxidizing biomarker TBARS
Quercitrin, a glycoside form of quercetin, prevents lipid peroxidation in vitro.
C Wagner, R Fachinetto, CL Dalla Corte, VB Brito, D Severo, G de Oliveira Costa Dias, AF Morel, CW Nogueira, JB Rocha
Centro de Ciências Naturais e Exatas, Departamento de Química, Programa de Pós-Graduação Bioquímica Toxicológica, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. Reactive oxygen species have been demonstrated to be associated with a variety of diseases including neurodegenerative disorders. Flavonoid compounds have been investigated for their protective action against oxidative mechanisms in different in vivo and in vitro models, which seems to be linked to their antioxidant properties. In the present study, we examine the protective mechanism of quercitrin, a glycoside form of quercetin, against the production of TBARS induced by different agents. TBARS production was stimulated by the incubation of rat brain homogenate with Fe(2+), Fe(2+) plus EDTA, quinolinic acid (QA), sodium nitroprusside (SNP) and potassium ferricyanide ([Fe(CN)(6)](3-)). Quercitrin was able to prevent the formation of TBARS induced by pro-oxidant agents tested; however, it was more effective against potassium ferricyanide ([Fe(CN)(6)](3-), IC(50) = 2.5), than quinolinic acid (QA, IC(50) = 6 mug/ml) and sodium nitroprusside (SNP, IC(50) = 5.88 mug/ml) than Fe(2+) (Fe(2+), IC(50) = 14.81 mug/ml), Fe(2+) plus EDTA (Fe(2+) plus EDTA, IC(50) = 48.15 mug/ml). The effect of quercitrin on the Fenton reaction was also investigated (deoxyribose degradation). Quercitrin caused a significant decrease in deoxyribose degradation that was not dependent on the concentration. Taken together, the data presented here indicate that quercitrin exhibits a scavenger and antioxidant role, and these effects probably are mediated via different mechanisms, which may involve the negative modulation of the Fenton reaction and NMDA receptor.
Quercitrin, a glycoside form of quercetin, prevents lipid peroxidation in vitro.
C Wagner, R Fachinetto, CL Dalla Corte, VB Brito, D Severo, G de Oliveira Costa Dias, AF Morel, CW Nogueira, JB Rocha
Centro de Ciências Naturais e Exatas, Departamento de Química, Programa de Pós-Graduação Bioquímica Toxicológica, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. Reactive oxygen species have been demonstrated to be associated with a variety of diseases including neurodegenerative disorders. Flavonoid compounds have been investigated for their protective action against oxidative mechanisms in different in vivo and in vitro models, which seems to be linked to their antioxidant properties. In the present study, we examine the protective mechanism of quercitrin, a glycoside form of quercetin, against the production of TBARS induced by different agents. TBARS production was stimulated by the incubation of rat brain homogenate with Fe(2+), Fe(2+) plus EDTA, quinolinic acid (QA), sodium nitroprusside (SNP) and potassium ferricyanide ([Fe(CN)(6)](3-)). Quercitrin was able to prevent the formation of TBARS induced by pro-oxidant agents tested; however, it was more effective against potassium ferricyanide ([Fe(CN)(6)](3-), IC(50) = 2.5), than quinolinic acid (QA, IC(50) = 6 mug/ml) and sodium nitroprusside (SNP, IC(50) = 5.88 mug/ml) than Fe(2+) (Fe(2+), IC(50) = 14.81 mug/ml), Fe(2+) plus EDTA (Fe(2+) plus EDTA, IC(50) = 48.15 mug/ml). The effect of quercitrin on the Fenton reaction was also investigated (deoxyribose degradation). Quercitrin caused a significant decrease in deoxyribose degradation that was not dependent on the concentration. Taken together, the data presented here indicate that quercitrin exhibits a scavenger and antioxidant role, and these effects probably are mediated via different mechanisms, which may involve the negative modulation of the Fenton reaction and NMDA receptor.