Extraction of polyphenols from Potentilla fruticosa L. as α-glucosidase inhibitors

Figures & data

Table 1. Identification and quantification of polyphenols in PL.

Compound	Molecular formula	Identification	Concentration (μg/g)
1	C21H24O11	(+)-Catechin-7-O-glucoside	6.1
2	C15H14O6	(+)-Catechin	3.4
3	C21H18O13	Quercetin 3-O-β-D-glucuronide	2.4
4	C26H28O16	Quercetin 3-vicianoside	0.7
5	C21H18O13	Quercetin 7-O-β-D-glucuronide	6.5
6	C15H10O7	Quercetin	1.2
7	C15H12O5	Naringenin	0.3
8	C21H22O11	(2S)-Eriodictyol-7-O-β-D-glucopyranoside	1.1
9	C21H22O11	(2R)-Eriodictyol 7-O-β-D-glucopyranoside	1.1
10	C43H48O22		0.4
11	C30H26O10	Afzelechin-(4α→8)-afzelchin	0.9
12	C31H28O12	bis-6,8’-Catechinylmethane	0.7
13	C31H28O12	bis-8,8’-catechinylmethane	1.8
14	C13H16O10	1-O-Galloyl-β-D-glucose	0.49
15	C20H20O14	1,6-di-O-Galloyl-β-D-glucose	0.98
16	C27H24O18	3,4,6-tri-O-Galloyl-β-D-glucose	0.8
17	C34H28O22	1,2,3,6-tetra-O-Galloyl-β-D-glucose	1.71
18	C7H6O4	Protocatechuic acid	0.4
19	C8H8O5	Methyl gallate	2.1
20	C7H6O5	Gallic acid	1.1
21	C10H12O2	(p-Hydroxybenzyl) acetone	0.4
22	C9H8O	Caffeic acid	0.4
23	C9H8O3	Naringeninic acid	1.0
24	C8H8O4	3-Methoxysalicylic acid	0.28
25	C7H6O4	5-Hydroxysalicylic acid	0.5
26	C9H10O2	3-Methyl-5-(2-propen-1-yl)-1,2-benzenediol	0.2
27	C7H6O4	3-Mydroxysalicylic acid	0.14
28	C10H8O2	1,8-Dihydroxynaphthalene	0.16
29	C12H16O6	Phenyl glucuronide	0.4
30	C16H22O7	Raspberry ketone β-D-glucoside	0.24
31	C12H16O7	Arbutin	0.37
32	C12H16O8	2,5-Dihydroxyphenyl-β-D-glucopyranoside	0.73
33	C13H8O8	Brevifolincarboxylic acid	0.9
34	C14H10O8	Brevifolincarboxylic acid methylester	0.9
35	C16H14O10		0.4
37	C16H18O9	Chlorogenic acid	1.47
38	C17H20O9	Chlorogenic acid methyl easter	0.96
39	C26H34O11	7S,8R-Dihydrodehydrodiconiferylalcohol 9-O-β-D-glucopyranoside	0.2
40	C20H24O8	1-[2,3-Dihydro-2-(4-hydroxy-3-methoxyphenyl)-3-(hydroxymethyl)-7-methoxy-5-benzofuranyl]-1,2,3-propanetriol	0.3
41	C36H58O11	Clethric acid 28-O-β-D-glucopyranosyl ester	0.5
42	C36H58O11	Niga-ichigoside F2	0.5

Table 2. Effect of PL extraction on glucose consumption of IECs.

Samples	Glucose consumption rate (%)
Normal	15.18 ± 1.44
Insulin	3.11 ± 1.19
Acarbose	29.11 ± 1.07
13	28.66 ± 2.31
9	28.05 ± 1.40
12	28.04 ± 1.65
5	26.95 ± 1.34
16	26.80 ± 1.34
8	26.75 ± .36
17	26.73 ± 1.66
7	26.64 ± 1.60
6	26.42 ± 1.47
11	26.11 ± 1.55
28	25.88 ± 1.49
23	24.73 ± 2.10
24	24.18 ± 1.54
20	24.11 ± 2.11

Table 3. In vitro inhibitory activity of compounds against α-glucosidase, type of inhibition and molecular docking binding energy.

Samples	IC50 (mg/mL)	Inhibitor type	Binding energy (kcal/mol)
Normal	2.895 ± 0.0056	competitive	-
insulin	0.02 ± 0.001	competitive	-
acarbose	0.047 ± 0.0012	competitive	−8.2
5	0.115 ± 0.0016	competitive	−10.9
6	0.395 ± 0.0026	competitive	−9.9
7	0.274 ± 0.0026	non-competitive	−10
8	0.215 ± 0.0036	mix	−10.4
9	0.07 ± 0.0014	mix	−11.6
11	0.827 ± 0.0082	competitive	−8.8
12	0.079 ± 0.0012	competitive	−11.3
13	0.063 ± 0.0015	mix	−11.9
16	0.128 ± 0.0016	non-competitive	−10.8
17	0.259 ± 0.0036	competitive	−10.3
20	0.982 ± 0.0028	competitive	−6.9
23	0.915 ± 0.0028	competitive	−7.5
24	0.963 ± 0.0028	competitive	−7.2
28	0.831 ± 0.0038	competitive	−8.5

Figure 1. Lineweaver-Burk plots for kinetic analysis of α-glucosidase inhibition. 5;6;7;8;9;11;12;13;16;17;20;23;24;28 represent the kinetic Lineweaver-Burk plots for the inhibition of α-glucosidase by different compounds, respectively, and the specific compound names are shown in Table 1.

Figure 2. Compound molecular docking and binding 3D diagram. 5;6;7;8;9;11;12;13.16;17;20;23;24;28 denote different compounds docked with α-glucosidase, respec-tively, and the specific compound names are shown in Table 1.