Preparative Lc Synthesis

purified through preparative LC as described above and finally characterized as phloretin and phloridzin (Fig. 1).
Compound 1 3-(4-hydroxyphenyl)-1-(2,4,6-trihydroxyphenyl)propan-1-one or phlorizin was obtained as amorphous powder, mp 2620C. The UV/Visible spectrum of the compound showed λmax at 225 and 285 nm. ESI–MS m/z 297 [M+Na]+ in positive ion mode and 273 [M-H] in negative ion mode for molecular formula C15H14O5; 274.
Compound 2 Commonly known as phlorizin. IUPAC name is 1-[2,4-dihydroxy-6-[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydropyran-2-yl]oxy-phenyl]-3-(4-hydroxyphenyl)propan-1-one was obtained as white to offwhite needle shaped crystals mp 1670C. The UV/Visible spectrum of the compound showed λmax at 226

The total run time was 25.0 min. Regression equations revealed good linear relationships for Pt and Pz (correlation coefficients: 0.9986 and 0.9989 respectively). This assay offers advantages in terms of practicality and suitability for the analysis of phloretin and phloridzin with acceptable validation results such as linearity, sensitivity, and recovery in terms of RSD (%).The method was linear in the concentration range of 50–500 ng/mL. The limit of quantification (LOQ) and limit of detection (LOD) was 68.74 ng and 20.62 ng for compound 1(PT) and 61.89 ng and 18.57 ng for compound

Glial cells are the primary central nervous system immune effector cells. Neuroinflammation is an altered situation developed in the presence of plays a significant role in various chronic and acute pathological conditions of the central nervous system. Our results showed that the stimulation of C6 cells with LPS (0.5 μg/mL) significantly increased the level of TNF-α and IL-6 in culture supernatant when compared with unstimulated cells (Fig. 3). It is well established that glial cells are the resident innate immune cells of the central nervous system, plays a critical role in inflammation-mediated neurodegeneration disorders. Lipopolysaccharide (LPS), an endotoxin, the outer membrane component of Gram-negative bacteria, is a major pathogenic factor in sepsis. LPS has been established for inflammatory research because LPS induces systemic inflammation mimicking the initial clinical features of sepsis (Block & Hong 2005). Both PZ and PT at the studied concentrations, i.e., 5 and 10 μg/mL, showed significant reduction in production of pro-inflammatory cytokines in LPS-induced neuroinflammation model in C6 cells. PZ showed 26.27±1.33 and 30.77±0.94 % inhibition and PT showed 17.10±1.19 and 42.13±3.54 % inhibition of TNF-α at dose 5 and 10µg/ml respectively. Similarly, PZ