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Page 6 of 9 Torres et al. Plast Aesthet Res 2020;7:57 I http://dx.doi.org/10.20517/2347-9264.2020.87

Table 1. Most extensively studied botanicals for photoprotection
Botanical agent Spectrum Mechanism of photoprotection Routes Models
Polypodium UVB, VL + Antioxidant: Augments natural antioxidant system, can scavenge Oral In vitro, mouse,
leucotomos extract UVA1, IR-A superoxide anion human
Anti-inflammatory: Increases MED, dose required for IPD, and
minimal phototoxic dose; inhibits proinflammatory transcription
factors, mediators, and cytokines; decreases VL + UVA1 induced
PPD and DT
Immunomodulatory: Preserves eLCs
Anti-tumor: Increases expression of p53 tumor suppressor gene
Anti-aging: Downregulates MMP; upregulates TIMP; prevents VL
and IR-A induced cell death and collagen degradation
Other: Suppresses photodermatoses
Green tea UVB Increases skin elasticity and blood flow; stimulates IL-12; decreases Topical, oral In vitro, mouse,
apoptosis, CPDs, sunburn, and TEWL; inhibits AP-1, NFKB, MAPK human
Pomegranate UVB Increases MED, skin moisture, and tumor latency; decreases Topical, oral Mouse, human
inflammation and multiplicity of tumors; inhibits ROS, erythema,
burning, DNA damage, cell proliferation, apoptosis, and collagen
breakdown
Resveratrol UVB Increases cell viability; decreases apoptosis, erythema, and Topical, oral In vitro, mouse,
(Grape seed, grape sunburn cell formation; inhibits COX, ornithine carboxylase, TGF human
peel, and red wine) beta, and NF-κB
Curcumin UVA, UVB Prevents ROS accumulation; decreases apoptosis, inflammation, Topical, oral In vitro, mouse,
(Turmeric) MMP-1 expression, and SCC tumor growth; inhibits NF-κB and human
MAPK
Silymarin UVA, UVB Activates p53 tumor suppressor gene; decreases MMP-1 NA In vitro
(Milk Thistle) activation, inflammation, ROS, DNA damage, apoptosis, IL-10, and
CPDs; inhibits collagenase, hyaluronidase, and elastase
UVB: ultraviolet B; UVA: ultraviolet A; VL + UVA1: visible light + ultraviolet A1; IR-A: infrared A; MED: minimal erythema dose; IPD:
immediate pigment darkening; PPD: persistent pigment darkening; DT: delayed tanning; eLCs: epidermal Langerhans cells; MMP:
matrix metalloproteinase; TIMP: tissue inhibitor of metalloproteinase; IL: interleukin; CPD: cyclobutane pyrimidine dimers; TEWL:
transepidermal water loss; AP-1: activator protein 1; NFKB: nuclear factor kappa B; MAPK: mitogen-activated protein kinase; ROS:
reactive oxygen species; DNA: deoxyribonucleic acid; COX: cyclooxygenase; TGF: tumor growth factor; SCC: squamous cell carcinoma;
NA: not applicable

chiefly marketed as an oral hepatic supplement and has been used to treat hepatitis, alcoholic liver
diseases, cirrhosis, and toxin-induced hepatotoxicity. The polyphenols present in silymarin, which
is more appropriately termed flavonolignans, are silybin, silychristin, silydianin, isosilybin, and
2,3-dehydrosilybin [32-34] .

The antioxidant and anti-inflammatory effects of silymarin are similar to other phenolic compounds in
that it downregulates the UVB-induced generation of ROS, expression of inflammatory transcription
factors and cytokines (e.g., TNF, IL-1, and iNOS), and activation of inflammatory pathways including
COX and lipoxygenase pathways. As an immunomodulatory compound, silymarin reverses UVB-induced
immunosuppression through decreased production of IL-10, which has been found to be elevated in the
presence of cancers and are thought to be responsible for the cancer’s ability to evade the host’s immune
response. In addition, silymarin imparts protection against UVB photocarcinogenesis through activation of
[34]
p53, and reduction of pyrimidine photoproduct formation .
In terms of protection against UVA, one in vitro study on human dermal fibroblasts revealed that pre-
treatment with silymarin one hour prior to UVA exposure decreased ROS production, DNA strand breaks,
activation of MMP-1, and the pro-apoptotic protein caspase-3 . In another in vitro study, silymarin and its
[35]
flavonolignans were found to inhibit the UVA-induced activity of collagenase, hyaluronidase, and elastase,
which are respectively responsible for skin wrinkling, loss of hydration, and sagging, indicating an anti-
[33]
photoaging effect .

[36]
However, a study by Fidrus et al. (2019) showed contradictory results wherein silymarin pre-treatment of
human keratinocytes in vitro 30 min prior to UVA exposure enhanced UVA-induced cytotoxicity in a dose