| Summary: | α-glucosidase is responsible for the hydrolysis of complex carbohydrates into simple absorbable glucose and causes postprandial hyperglycemia. α-glucosidase inhibition is thus the ideal target to prevent postprandial hyperglycemia. The present study was therefore designed to analyze the effects of various compounds isolated from <i>Dryopteris cycadina</i> against α-glucosidase including β-Sitosterol <b>1</b>, β-Sitosterol3-<i>O</i>-β-<span style="font-variant: small-caps">d</span>-glucopyranoside <b>2</b>, 3, 5, 7-trihydroxy-2-(<i>p</i>-tolyl) chorman-4-one <b>3</b>, Quercetin-3-0-β-<span style="font-variant: small-caps">d</span>-glucopyranoside (3<sup>/</sup>→0-3<sup>///</sup>)- β-<span style="font-variant: small-caps">d</span>- Quercetin -3-0- β –<span style="font-variant: small-caps">d</span>-galactopyranoside <b>4</b> and 5, 7, 4<sup>/</sup>-Trihydroxyflavon-3-glucopyranoid 5. The in vitro spectrophotometric method was used for the analysis of test compounds against possible inhibition. Similarly, molecular docking studies were performed using the MOE software. These compounds showed concentration-dependent inhibition on α-glucosidase, and compounds <b>1</b> (IC<sub>50</sub>: 143 ± 0.47 µM), <b>3</b> (IC<sub>50</sub>:133 ± 6.90 µM) and <b>5</b> (IC<sub>50</sub>: 146 ± 1.93 µM) were more potent than the standard drug, acarbose (IC<sub>50</sub>: 290 ± 0.54 µM). Computational studies of these compounds strongly supported the in vitro studies and showed strong binding receptor sensitivity. In short, the secondary metabolites isolated from <i>D. cycadina</i> demonstrated potent α-glucosidase inhibition that were supported by molecular docking with a high docking score.
|
|---|