Table 1.
Phytocompound | Source | In vitro Method/Model | Biological Activity | Reference |
---|---|---|---|---|
Betulinic acid | Dillenia indica | Lipid peroxidation test/egg yolk | Protection against lipid peroxidation | [2] |
Diospyros kaki | Lipopolysaccharide-stimulated RAW264.7 macrophages | HO-1/Nrf2 translocation suppressing the NF-κB pathway | [3] | |
Pure compound |
Rat cardiomyocyte-derived H9c2 cell/hypoxia/reoxygenation (H/R) model | Protection against myocardial ischemia reperfusion injury | [4] | |
Betulin | Birch bark | Human keratinocytes | Keratinocyte migration, increase of pro-inflammatory mediators | [5] |
Lupeol |
Bowdichia virgilioides Pure compound |
Epidermal keratinocytes and dermal fibroblasts/scratch wound healing assay UVA radiated dermal fibroblast |
Enhancement in migration and wound closure and contraction of dermal fibroblasts; regulation via PI3K/Akt and MAPK pathways Anti -aging effects by inhibiting p16, p21 and p-p53 and decreasing the MMP-1, -2, -3 expression. |
[6,7] |
Asiaticoside | Pure compound |
Human dermal fibroblasts, human epidermal keratinocytes |
increased migration rates of skin cells; enhance the initial skin cell adhesion; increase in the number of normal human dermal fibroblasts | [8] |
Pure compound |
Human dermal fibroblasts | Increases the synthesis of type I collagen by activation of the Smad pathway | [9] | |
Centella asiatica | HaCaT keratinocytes | Pro-migratory effect; upregulation of signaling pathways involved in wound healing:FAK, Akt, and MAPK | [10] | |
Pure compound |
Keloid primary fibroblast cultures | Inhibition of keloid fibroblasts proliferation and prevention of excessive scarring | [11,12] | |
Asiatic acid | Pure compound |
Primary keloid and normal fibroblasts | Keloid prevention by inhibiting TGF-β1-induced collagen expression via PPAR-γ activation | [13] |
Oleanolic acid | Viscum album | NIH/3T3 and HaCat cells/wound healing assay |
Enhanced wound closure by stimulation of the migration of fibroblasts | [14] |
Pure compound |
mink lung epithelial cells, MDA-MB-231 | Stimulation of cell migration by stimulation of mitogen-activated protein (MAP) kinases | [15] | |
Glycyrrhizin | Pure compound |
Normal human dermal fibroblasts | Reduction of fibrosis, increase of apoptosis and reduction of autophagy in keloids by HMGB1 inhibition | [16] |
Camellioside B | Camellia japonica | Normal human neonatal skin Fibroblasts |
Enhanced proliferation | [17] |
Perennisosides Asterbatanoside D Bernardioside B2, Bellissaponins | Bellis. perennis | Normal human dermal fibroblasts | Promotion of collagen synthesis | [18] |
Ginsenosides | Panax ginseng CA Meyer | Human dermal fibroblast cells | Healing effect, increase in type I collagen synthesis by activating the Smad pathway | [19] |
Pure compound |
HaCaT/wound scratch assay | Wound healing stimulation by increasing the migration of human keratinocytes through S1P dependent mechanism. | [20] | |
Cycloastragenol | Astragalus membranaceus | Human HaCaT keratinocytes and primary human dermal fibroblasts/Scratch wound test | Increase cell migration and proliferation by EGFR stimulation | [21] |
Pure compound |
Human epidermal stem cells EpSCs | Wound healing by stimulation of EPSCS proliferation and migration by activation of Wnt/β-catenin signaling | [22] | |
Astragaloside IV, Cyclocephaloside I Cyclocanthoside E | Pure compounds |
human keratinocytes/migration scratch assay | Wound healing by proliferation and migration | [23] |
Astragaloside VI | Astragalus membranaceus | Human HaCaT keratinocytes and primary human dermal fibroblasts | Stimulation of skin cell proliferation and migration by activation of EGFR, | [21] |