Table 1.

Presentation of the main mechanisms of action on skin diseases produced by species of the Rosaceae family.

Species	Anti-Inflammatory Mechanisms of Action	Targeted Skin Conditions	References
Eriobotrya japonica	↓ NF-κB, ↓ p38 MAPK, ↓ ERK	Inflammation, edema, acne	[76]
Filipendula palmata	↓ Chemokine genes/proteins (via MAPK and NF-κB pathways)	Burns, skin inflammation	[79]
Cydonia oblonga	↓ NF-κB, ↓ p38 MAPK, ↑ AKT, ↓ COX-2	General inflammation, skin aging	[81,82]
Pyrus ussuriensis	↓ NO, ↓ IL-6, ↓ IL-1β	Atopic dermatitis	[84]
Crataegus spp.	↓ TNF-α, ↓ IL-1β, ↓ IL-6, ↓ IL-33, ↓ NO, ↓ PGE2, ↑ IL-10	Chronic inflammation, wound healing	[85,86]
Rubus idaeus	↓ COX, ↓ LOX	Inflammatory and oxidative skin damage	[87]
Rosa damascena	↓ Inflammation gene Expression	Wound healing, antiaging	[88]
Cotoneaster spp.	↓ Hyaluronidase, ↓ COX-1/2, ↓ LOX, ↓ prostaglandins	Acne, oxidative stress, skin inflammation	[89,91]
Rosa multiflora	Downregulation of iNOS and COX-2 expression	Atopic dermatitis	[93]

↓—inhibition/decrease in activity or expression, ↑—activation/increase in activity, NF-κB—Nuclear Factor Kappa B, MAPK—Mitogen-Activated Protein Kinase, ERK—Extracellular Signal-Regulated Kinase, COX—cyclooxygenase (COX-1, COX-2), LOX—lipoxygenase, AKT—Protein Kinase B, NO—nitric oxide, TNF-α-—tumor necrosis factor-alpha, IL-1β—Interleukin-1 beta, IL-6—Interleukin-6, IL—Interleukin-33, PGE2—prostaglandin E2, ↑ IL-10—Interleukin-10.