Fig 1.
The scientific hypothesis of this study.
Fig 2.
The experimental protocol of this study.
(A) Cell biological experiments; (B) Chemical experiments.
Fig 3.
The extraction process of WNGH-AE.
Fig 4.
Cytocompatibility of different concentrations of WNGH-AE.
(A) MTT value (%) of different concentrations of WNGH-AE; (B) LDH value (U/L) of different concentrations of WNGH-AE. (****: indicates P<0.001, comparison with t-BHP group).
Fig 5.
Levels of the effect of WNGH-AE on ROS levels in HepG2 cells.
(A) Detection of cellular ROS level; (B) Detection of cellular 8-OHdG level; (* Indicates comparison with t-BHP group, **: P<0.01, ***: P<0.001.).
Fig 6.
Effect of WNGH-AE on the anti-oxidative stress capacity of HepG2 cells.
(A) Detection of cellular NF-κB level; (B) Detection of cellular TNF-α level; (C) Detection of cellular IL-1β level. (* Indicates comparison with t-BHP group, **: P<0.01, ***: P<0.001; # numbers indicate comparison with VC group, ###: P<0.001.).
Fig 7.
Antioxidant activity of WNGH extracts.
(A). Scavenging activity of different solvent extracts of WNGH against DPPH; (B). Scavenging activity of different solvent extracts of WNGH against ·OH.
Table 1.
Semi-inhibitory activity (IC50) of solvent extracts of WNGH against DPPH and ·OH radicals.
Table 2.
Total phenolic, flavonoid and polysaccharide content of WNGH-AE.
Fig 8.
(A): Positive ion flow diagram; (B): Negative ion flow diagram.
Fig 9.
Types and contents of compounds in WNGH-AE (Top 20).
Table 3.
LC–MS analysis of WNGH-AE.
Fig 10.
LC–MS analysis of WNGH-AE of number of KEGG pathway compounds.
Table 4.
LC–MS analysis of WNGH-AE of KEGG pathway.