resperidone cost Myricetin is tri hydroxylated at

Myricetin is tri-hydroxylated at positions 3′, 4′ and 5′, and shows one down field non-coupled aromatic hydrogen signal integrating for two protons, namely the H-2′ and H-6′ protons of the B-ring. This was seen in the 1H NMR of compound I at δ 7.09 ppm. The anomeric proton signal at δ 5.53 ppm indicated α-L-glycosidic configuration [25]; while the methyl proton signals at δ 1.06 ppm (d, J = 5.8 Hz) that coupled vicinal to the H-5″ proton, and the corresponding δ 17.7 ppm primary carbon signal, were diagnostic of rhamnoses [25]. The C3 δ 136.4 ppm confirmed the position of sugar linkage. Thus compound I was identified as a myricetin-3-O-α-l-rhamnopyranoside derivative. The 1H NMR shift of the C2″ carbon (δ 5.65 ppm) was more down field as should be expected for just myricetin-3-O-α-l-rhamnopyranoside, as observed in the 1H NMR of compound III at δ 4.22 ppm (dd, J = 1.7, 3.4); and thus indicated possible acylation at that position. This was supported by the C7‴ carbon 13C NMR signal at δ 165.1 ppm. The two proton singlet signals at δ 7.00 ppm and the corresponding two aromatic carbons δ 109.0 ppm 13C NMR signals, confirmed gallic resperidone cost as the acyl component; as initially suspected from the negative ion (NI) mass spectrum. Therefore, compound I was confirmed to be myricetin-3-O-(2″-O-galloyl)-α-l-rhamnopyranoside. Similarly, compound II was seen as an acylated flavonol glycoside; since the δ of the H-2″ hydrogen atom (5.63 ppm) was deshielded as observed in the 1H NMR of I, and compared to the corresponding value (4.22 ppm, dd, J = 1.7, 3.3 Hz) in compound IV. The 1H NMR of II was identical to that of I; except that its B-ring expressed three aromatic proton signals at δ 6.94 (d, J = 8.3 Hz), 7.35 (dd, J = 2.1, 8.3 Hz) and 7.37 ppm (d, J = 2.1 Hz), each integrating for one hydrogen atom. Coupling constants of the signals indicated an aromatic ABX system, where the signal at δ 7.35 ppm (dd, J = 2.1, 8.3 Hz) was ortho to signal δ 6.94 ppm (d, J = 8.3 Hz), and metha to signal δ 7.37 ppm (d, J = 2.1 Hz). This implied that the B-ring is diortho-hydroxylated at C3′ and C4′; and as such indicated that the aglycone is quercetin. The 1H NMR and 13C NMR data of II correlated well with published literature [27]. The isolated compound was identified as quercetin-3-O-(2″-O-galloyl)-α-l-rhamnopyranoside. The 1H NMR and 13C NMR signals of compounds III and IV correlated perfectly with the reported data [28,29]. This was further confirmed for IV by comparison to other literature [30]. Thus both compounds were described as myricetin-3-O-α-l-rhamnopyranoside and quercetin-3-O-α-l-rhamnopyranoside, respectively. 1H NMR and 13C NMR data of compound V was in agreement with typical quercetin chemical shifts. The sugar component 1H NMR signals of the flavonoid glycoside, however lacked either the terminal methyl hydrogen atoms signal usually associated with deoxyhexosides or the hydroxy methylene signals found in hexosides. Rather the 1H NMR spectrum indicated two germinal proton signals at 3.82 and 3.65 ppm; alongside other four distinct proton signals. This indicated a pentoside sugar moiety, as observed in the NI mass fragmentation of compound V. The broad singlet signal of the C4-H″ atom at δ 3.81 ppm confirmed an arabinopyranoside sugar moiety, while the absence of a broad singlet and a J constant of 1–2 Hz for the anomeric proton [5.17 ppm (d, J = 6.5)] eliminated the consideration of an alpha-l-arabinopyranoside configuration. Rather the δ value and the J constant indicated a beta-l-arabinopyranoside configuration. Thus compound V was identified as quercetin-3-O-β-l-arabinopyranoside. The isolated compounds are confirmed anti-bacterial, anti-hyperglycaemic and anti-cancer agents [27,31,32]. Quercetin, specifically, reduces blood pressure and endothelial dysfunction in animal models of hypertension, via a nitrogen oxide (NO) scavenging effect [33].