Skin Anti-Aging Support

Ultraviolet Radiation Causes Premature Skin Aging and Damage
    Natural Protection from Apigenin Luteolin Curcumin and Ginger


o Ultraviolet Radiation and Skin Aging (Photoaging)

The most potent source of aging for the skin is the ultraviolet radiation from solar UVA and UVB rays. UV radiation significantly degrades the connective tissue of the skin, the result of breakdown of the extracellular matrix of collagen and elastic fibers. The result is sagging skin, wrinkles, discoloration, inflammatory processes, oxidative stress and DNA damage of the skin cells. Whenever DNA is damaged, there is also increase likelihood for skin cancer, including melanoma.

Aging of skin is one of the first noticeable signs of aging and can make the most impact when trying to portray a younger image. Photoaging and photocarcinogenesis are the result of skin damage due to chronic UVA and UVB radiation exposure. While UVB is most intense during summer months, the intensity level of UVA rays remains at the same strength year-round. UVA rays also penetrate car windshields and office windows, which is why many people who NEVER GO OUT IN THE SUN, develop significant sun damage and skin cancers just through the act of driving or being by a window. UVA rays are also more skin damaging than UVB rays. UVB and UVA rays accelerate the aging of the skin and are a primary source of skin aging.

  • UVB Damage

UVB rays penetrate only the top layer of skin called the epidermis. Contained in this layer are keratinocytes (skin cells), basal cells and melanocytes. UVB stimulate melanocytes to produce melanin, which gives the skin a “tanning color” and freckles during periods of exposure to UVB rays. 
(1) UVB Strongly increases levels of COX-2 : a potent cancer initiator
(2) UVB stimulates an increased release of inflammatory mediators.
(3) UVB damages the cell and DNA and can lead to cancer.

• UVA Damage

UVA rays penetrate through the epidermis into the deeper layer of skin called the dermis. The dermis contains blood vessels, collagen and elastin support fibers, as well as youth enhancing binding substances.
(1) UVA damage can cause a breakdown of the collagen, elastin and binders, causing the epidermis layer to sag and wrinkle.
(2) Furthermore, UVA also permanently dilates the blood vessels in the dermis, creating a red appearance in the skin.
(3) UVA damages the cell and DNA and can lead to skin cancer.


o Natural yellow compounds and Skin Protection

Natural yellow compound including luteolin, apigenin, curucmin and ginger have shown promising potential for protecting the skin against both UVA and UVB damage. both the neutralizing of immediate UVA and UVB damage, and reversing some of the effects of already damaged skin.

Luteolin and Apigenin Luteolin and apigenin have been shown as skin protectors from harmful UV radiation in many research studies (using both cellular culture and live animals).

• In UVB radiation exposure, luteolin was shown to effectively diminish UVB induced DNA-damage, reduce inflammation, and suppress increases in UVB induced COX-2. (1)
• In another study involving mice and cell cultures, luteolin inhibited the incidence of UVB-induced skin cancer.(2)
• Luteolin is also shown to inhibit cellular death of normal skin cells and inhibited the release of inflammatory mediators in response to UVB-induced experimental sunburn.(3)
• Apigein inhibits UVB induced COX-2 upregulation.(4) Studies also show that apigenin is an inhibitor of skin cancer.
• Both apigenin and luteolin inhibit matrix metalloproteinases (MMPs). MMPs cause skin aging by degrading the extracellular matrix proteins (including collagen and elastin fibers) in the dermis layer of the skin. These enzymes are activated by UVA radiation, and significantly age the appearance of the skin. (5) It is also suggested by researchers that the destruction of collagen in the dermis is a causative factor in skin cancer.

Green Tea Extract and Ginger

• Green tea polyphenols rapidly repairs UVB damaged DNA, and has been shown to prevent UBV induced non-melanoma skin cancer on lab animals.(6)
• Green tea polyphenols inhibit UVB-induced inflammatory responses, immunosuppression and oxidative stress.(7) Conclusions of researchers is that green tea polyphenols offer significant photo protection and can potentially be used in prevention of UVB induced skin damage.
• EGCG significantly protects skin cells against UVB radiation. EGCG inhibited lipid peroxidation of cell membranes and cytotoxic H202 generation in the skin cells.(8)
• Gingerol extract from ginger was shown in cultured cells and in live mice, to attenuate the UVB induced inflammatory response in UV damaged skin cells. When gingerol was administered to UVB damaged skin cells, gingerol attenuated UVB induced damage, including cell viability, hyperplasia, and blood vessel dilation in dermis. (9) Other studies indicate that gingerol reduces UBV-induced intracellular reactive oxygen species (ROS) levels and COX-2 activation.(10)

Curcumin UV damaged skin frequently also involved damaged DNA which can lead to skin cancer. Curcumin’s ability to attenuate oxidative stress levels and suppress inflammation of the radiation skin injury, provides a basis for anti-photoaging and anti-carcinogenesis therapy. Researchers suggest that curcumin may be able to repair photodamaged skin, thereby inhibiting progression of the damaged skin to cancer. (11)


o Anti-Skin Carcinogenesis / Anti-Skin Cancer

Yellow anti-aging compounds are among the most potent natural inhibitors of skin cancer. Research using both cell cultures and live animals have validated the potential for yellow anti-aging to target initiation of skin cancer and the inhibition of the progression.

• Apigenin Research: (12), (13)          Luteolin Research: (14), (2)
• Fisetin Research: (15)                       Pterostilbene Research: (16)
• Curcumin Research: (17), (11)        Green Tea Research: (18), (19)
• Ginger Research: (20), (21)



(1) Wölfle U, et al. UVB-induced DNA damage, generation of reactive oxygen species, and inflammation are effectively attenuated by the flavonoid luteolin in vitro and in vivo. Free Radic Biol Med. 2011 May 1;50(9):1081-93.
(2) Byun S, et al. Luteolin inhibits protein kinase C(epsilon) and c-Src activities and UVB-induced skin cancer. Cancer Res. 2010 Mar 15;70(6):2415-23.
(3) Verschooten L, et al. The flavonoid luteolin increases the resistance of normal, but not malignant keratinocytes, against UVB-induced apoptosis. J Invest Dermatol. 2010 Sep;130(9):2277-85.
(4) Van Dross RT, et al. Modulation of UVB-induced and basal cyclooxygenase-2 (COX-2) expression by apigenin in mouse keratinocytes: role of USF transcription factors. Mol Carcinog. 2007 Apr;46(4):303-14.
(5) Hwang YP, et al. The flavonoids apigenin and luteolin suppress ultraviolet A-induced matrix metalloproteinase-1 expression via MAPKs and AP-1-dependent signaling in HaCaT cells. J Dermatol Sci. 2011 Jan;61(1):23-31.
(6) Kativar SK. Green tea prevents non-melanoma skin cancer by enhancing DNA repair. Arch Biochem Biophys. 2011 Apr 15;508(2):152-8.
(7) Kavitar SK. Skin photoprotection by green tea: antioxidant and immunomodulatory effects. Curr Drug Targets Immune Endocr Metabol Disord. 2003 Sep;3(3):234-42.
(8) Huang CC, et al. (-)-Epicatechin-3-gallate, a green tea polyphenol is a potent agent against UVB-induced damage in HaCaT keratinocytes. Molecules. 2007 Aug 14;12(8):1845-58.
(9) Guahk GH, et al. Zingiber officinale protects HaCaT cells and C57BL/6 mice from ultraviolet B-induced inflammation. J Med Food. 2010 Jun;13(3):673-80.
(10) Kim JK, et al. [6]-Gingerol prevents UVB-induced ROS production and COX-2 expression in vitro and in vivo. Free Radic Res. 2007 May;41(5):603-14.
(11) Heng MC, et al. Curcumin targeted signaling pathways: basis for anti-photoaging and anti-carcinogenic therapy. Int J Dermatol. 2010 Jun;49(6):608-22.
(12) Shukla S, et al. Apigenin: a promising molecule for cancer prevention. Pharm Res. 2010 Jun;27(6):962-78.
(13) Balasubramanian S, et al. Apigenin inhibition of involucrin gene expression is associated with a specific reduction in phosphorylation of protein kinase Cdelta Tyr311. J Biol Chem. 2006 Nov 24;281(47):36162-72.
(14) Seelinger G, et al. Anti-carcinogenic effects of the flavonoid luteolin. Molecules. 2008 Oct 22;13(10):2628-51.
(15) Arbiser JL, et al. Fisetin: a natural fist against melanoma? J Invest Dermatol. 2011 Jun;131(6):1187-9.
(16) Ferrer P, et al. Association between pterostilbene and quercetin inhibits metastatic activity of B16 melanoma. Neoplasia. 2005 Jan;7(1):37-47.
(17) Phillips JM, et al. Curcumin Inhibits Skin Squamous Cell Carcinoma Tumor Growth In Vivo. Otolaryngol Head Neck Surg. 2011 Mar 1.
(18) Yang CS, et al. Cancer prevention by tea: Evidence from laboratory studies. Pharmacol Res. 2011 Aug;64(2):113-22.
(19) Nandakumar V, et al. (-)-Epigallocatechin-3-gallate reactivates silenced tumor suppressor genes, Cip1/p21 and p16INK4a, by reducing DNA methylation and increasing histones acetylation in human skin cancer cells. Carcinogenesis. 2011 Apr;32(4):537-44.
(20) Nigam N, et al Induction of apoptosis by [6]-gingerol associated with the modulation of p53 and involvement of mitochondrial signaling pathway in B[a]P-induced mouse skin tumorigenesis. Cancer Chemother Pharmacol. 2010 Mar;65(4):687-96.
(21) Nigam N, et al. [6]-Gingerol induces reactive oxygen species regulated mitochondrial cell death pathway in human epidermoid carcinoma A431 cells. Chem Biol Interact. 2009 Sep 14;181(1):77-84.