# Phytochemical Composition, Antioxidant and Anti-Inflammatory Activities, and Protective Effect Against LPS-Induced Liver Injury in Mice of Gerbera delavayi Franch

**Authors:** Hongmei Yin, Yinrong Zhao, Rouxian Hu, Jing Yang, Yuanhang Chen, Huaqiao Tang, Xiaoyan Li, Gang Ye, Fei Shi, Cheng Lv, Ling Zhao

PMC · DOI: 10.3390/antiox15010143 · Antioxidants · 2026-01-22

## TL;DR

This study shows that Gerbera delavayi extract has antioxidant and anti-inflammatory properties and protects against liver damage in mice.

## Contribution

The study identifies the phytochemical composition and demonstrates the hepatoprotective effects of Gerbera delavayi for the first time.

## Key findings

- E-GDF contains high levels of flavonoids and polyphenolic compounds with strong antioxidant activity.
- E-GDF reduces inflammation and ROS production in LPS-stimulated macrophages and lowers liver injury markers in mice.
- E-GDF ameliorates LPS-induced liver damage and shows potential as a hepatoprotective herbal medicine.

## Abstract

The main objective of this study was to preliminarily analyze the major flavonoid and phenolic acid components of the ethanolic extract of Gerbera delavayi Franch (E-GDF), and to evaluate its anti-inflammatory and antioxidant properties in lipopolysaccharide (LPS)-stimulated murine macrophage RAW264.7 cells and systemic inflammation mouse models. Results indicated that E-GDF was rich in flavonoids (16.35 ± 0.19 mg RT/g d.w. Plant Material) and polyphenolic compounds (36.15 ± 0.20 mg GAE/g d.w. Plant Material). LC-MS analysis of E-GDF revealed that its major flavonoid components included kaempferol glycosides, luteolin, and their glycosylated derivatives, while its phenolic acids were predominantly chlorogenic acid, caffeic acid, ferulic acid, and their corresponding glycosides. E-GDF exhibited good antioxidant activities, including the scavenging of DPPH, ABTS, •OH, and O2•− radicals. E-GDF treatment significantly inhibited the production of ROS and inflammatory mediators (NO, IL-6, TNF-α) in LPS-stimulated macrophages (RAW 264.7), while concurrently down-regulating the mRNA expression of COX-2, IL-1β, Casp1, and GSDMD-1. In addition, in vivo experiments revealed that E-GDF treatment effectively reduced the serum LPS, AST levels, as well as hepatic TNF-α, IL-6 levels in mice with LPS-induced acute liver injury. Furthermore, E-GDF significantly ameliorated LPS-induced liver pathological damage. These results provide a basis for G. delavayi as a potential antioxidant, anti-inflammatory, and hepatoprotective herbal medicine.

## Linked entities

- **Chemicals:** ABTS (PubChem CID 35688), •OH (PubChem CID 961), O2•− (PubChem CID 977), NO (PubChem CID 24822), IL-6 (PubChem CID 165368475)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, Casp1 (caspase 1) [NCBI Gene 12362] {aka ICE, Il1bc}, COX2 (cytochrome c oxidase subunit II) [NCBI Gene 17709], Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, Slc17a5 (solute carrier family 17 (anion/sugar transporter), member 5) [NCBI Gene 235504] {aka 4631416G20Rik, 4732491M05, AST, ISSD, NSD, SD}
- **Diseases:** Liver Injury (MESH:D017093), Inflammatory (MESH:D007249), liver pathological damage (MESH:D056486), acute liver injury (MESH:D017114)
- **Chemicals:** GAE (-), luteolin (MESH:D047311), caffeic acid (MESH:C040048), ABTS (MESH:C002502), NO (MESH:D009614), flavonoid (MESH:D005419), ferulic acid (MESH:C004999), LPS (MESH:D008070), chlorogenic acid (MESH:D002726), OH (MESH:C031356), DPPH (MESH:C004931), phenolic acid (MESH:C017616), glycosides (MESH:D006027)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12837755/full.md

## References

42 references — full list in the complete paper: https://tomesphere.com/paper/PMC12837755/full.md

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Source: https://tomesphere.com/paper/PMC12837755