Silymarin As an Anti-Inflammatory and Inhibitor of UV-Induced Skin Damage

It is a well-known fact of life that exposure to UV light, especially the UVA component, festers skin disorders like melanoma and non-melanoma skin cancers. Superficial remedies such as sunscreens are effective only to a limited extent. This realization has led to investigation of new methods to protect the skin from photo-damaging effects of solar UV radiation, or “photo-carcinogenesis” as it is called. Recent years have seen considerable interest in identifying naturally-occurring botanicals, such as silymarin, with anti-oxidant and anti-inflammatory properties, and which exhibit anti-carcinogenic and anti-mutagenic functionality.

It is in this light that the medicinal benefits of milk thistle have been a subject of intense research by scientists. Though its value as a medicine for a host of health conditions, including dermatological, has been known for over 2,000 years, it is only now that science has seriously begun looking at the role played by milk thistle and “Silymarin”, its active compound, in treating skin damage.

In an experiment conducted at Palacky University in Czechoslovakia (1), researchers studied the impact of two components of Silybum marianum (technical name for milk thistle) as both a preventative as well as treatment intervention for skin damage against UVA exposure. Their findings were positive, in that it was discovered that these two components – collectively known as “flavonolignans” – perform a host of functions, such as increasing the viability of keratinocytes in irradiated cells, inhibiting the production of ROS, stopping further depletion of ATP and GSH taking place at intracellular level, and halting the peroxidation of membrane lipids. Further, the activation of caspases-3 process that UVA exposure initiates gets halted and reversed when the two components of Silybum marianum are applied. The overall picture that emerges, therefore, is that Silybum marianum is a good candidate to be considered for inhibiting UV damage.

An interesting experiment conducted on mice at the University of Alabama in Birmingham has been reported in the March-April 2008 issue of Photochem Photobiology journal (2). Two observations from this research are of special relevance to us here. One, it is the CD11b+ cells, which are the major source of oxidative stress in UV-irradiated skin, were inhibited by Silymarin. The flavonoid also suppresses the infiltration of leukocytes that UV exposure had induced. The second important observation is that Silymarin not only halts UV damage, it also acts as a preventive measure. Another researcher has gone one step ahead with the identification of yet another reversal that this chemical performs to UV action: it reduces the volume of H2O2-producing and cytokine interleukin-10 producing cells, both of whose generation is activated by UV (6).

Nearly the same conclusion has been arrived at by researchers working in the Department of Pharmaceutical Sciences at the University of Colorado (3). Their research has shown a positive effect of Silibinin on the repair of UVB-induced DNA damage. Another experiment conducted at the Department of Dermatology of the University of Alabama has observed the inhibition affect that the flavonoid has on tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate, mezerein, benzoyal peroxide and okadaic acid (4).

Topical application of Silibinin prior to, or immediately after, UV irradiation has been found to inhibit thymine dimer positive cell generation that UV induces in the epidermis (5). This research has also shown that terminal sunburn cell formation that is again induced by UV is inhibited too, when Silibinin is applied.

A strong case for Silymarin being a very effective agent in inhibiting and reversing carcinogen and tumor-promoter-induced cancers is made by two independent researches. In both the experiments (7), (8), it has been reported that Silibinin inhibits cancer-causing cells (ERK1/2 activation) and promotes benign cells (JNK1/2, p38), making it an effective cancer-intervention agent for cancer.

A paper published in the journal “Cancer Research” details yet another in-depth investigation carried out on the efficacy of Silymarin as a possible intervention agent against Stage I and Stage II tumors (9). The paper reports that the milk thistle extract has been found to be especially useful in Stage I tumor suppression, and inhibits edema, hyperplasia, proliferation index and oxidant state which take place due to UV irradiation. This same result has been arrived by an independent group of researchers, who used a different chemical to induce skin edema in mice (10).

From the above researches being conducted around the world, it may safely be concluded that Silymarin is proving to be very effective in inhibiting UV-induced skin damage, and the day may not be far when milk thistle becomes one of the major ingredients in sunscreen lotions.

References

Svobodová A, Zdarilová A, Walterová D, and Vostálová J. Flavonolignans from Silybum marianum moderate UVA-induced oxidative damage to HaCaT keratinocytes. J Dermatol Sci. 2007 Dec;48(3):213-24. Epub 2007 Aug 3.

Katiyar SK, Meleth S, and Sharma SD. Silymarin, a flavonoid from milk thistle (Silybum marianum L.) inhibits UV-induced oxidative stress through targeting infiltrating CD11b+ cells in mouse skin. Photochem Photobiol. 2008 Mar-Apr;84(2):266-71. Epub 2007 Nov 28.

Singh RP, and Agarwal R. Mechanisms and preclinical efficacy of silibinin in preventing skin cancer. Eur J Cancer. 2005 Sep;41(13):1969-79.

Katiyar SK. Silymarin and skin cancer prevention: anti-inflammatory, antioxidant and immunomodulatory effects. Int J Oncol. 2005 Jan;26(1):169-76.

Dhanalakshmi S, Mallikarjuna GU, Singh RP, and Agarwal R. Silibinin prevents ultraviolet radiation-caused skin damages in SKH-1 hairless mice via a decrease in thymine dimer positive cells and an up-regulation of p53-p21/Cip1 in epidermis. Carcinogenesis. 2004 Aug;25(8):1459-65. Epub 2004 Mar 19.

Katiyar SK. Treatment of Silymarin, a plant flavonoid, prevents ultraviolet light-induced immune suppression and oxidative stress in mouse skin. Int J Oncol. 2002 Dec;21(6):1213-22.

Singh RP, Tyagi AK, Zhao J, and Agarwal R. Silymarin inhibits growth and causes regression of established skin tumors in SENCAR mice via modulation of mitogen-activated protein kinases and induction of apoptosis. Carcinogenesis. 2002 Mar;23(3):499-510.

Jifu Zhao, Moushumi Lahiri-Chatterjee, Yogesh Sharma and Rajesh Agarwal. Inhibitory effect of a flavonoid antioxidant Silymarin on benzoyl peroxide-induced tumor promotion, oxidative stress and inflammatory responses in SENCAR mouse skin. Carcinogenesis, Vol. 21, No. 4, 811-816, April 2000.

Lahiri-Chatterjee M, Katiyar SK, Mohan RR, and Agarwal R. A flavonoid antioxidant, Silymarin, affords exceptionally high protection against tumor promotion in the SENCAR mouse skin tumorigenesis model. Cancer Res. 1999 Feb 1;59(3):622-32.

Zhao J, Sharma Y, and Agarwal R. Significant inhibition by the flavonoid antioxidant Silymarin against 12-O-tetradecanoylphorbol 13-acetate-caused modulation of antioxidant and inflammatory enzymes, and cyclo-oxygenase-2 and interleukin-1-alpha expression in SENCAR mouse epidermis: implications in the prevention of Stage I tumor production. Mol Carcinog. 1999 Dec;26(4):321-33.

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5 Melanoma Facts Which You Must Know

It is widely known that melanoma is the deadliest of skin cancers. However, people are still not well familiar with important facts about this condition. At the same time, this information is extremely valuable and may help to save lives. Get better informed now so that you can start taking better measures for protection without delay.

It is among the most common types of cancer in young people.

Melanoma typically holds the first or second place in the national charts for the most widely spread types of cancer in the age group from 15 to 39. It is also among the deadliest types affecting young people. Given this, young people as well as older adults need to take adequate measures for prevention including regular mole checks.

Frequent sunbed use increases the risk of melanoma.

The regular use of sunbeds, typically more than 10 times a year, can increase the risk of developing this type of skin cancer by as much as 74%. This is because the UV radiation produced by these facilities penetrates the skin much more deeply compared to the rates of the sun. As a result, it causes greater damage to the skin cells. Your best bet is to stay away from sunbeds.

Clothing does not offer full protection from the sun’s UV rays which cause skin cell damage.

It is true that clothes made from light tightly woven fabrics in light colours provide some protection, but it is not complete. That is why your best bet is to seek the shade between 11 in the morning and 5 in the afternoon. If this is not always possible, you should apply sunscreen even on areas of the skin which are covered by clothing. Just let the cream or lotion get fully absorbed before you put your clothes on.

Cancerous growths can appear anywhere on the skin.

It is a huge misconception that melanoma can develop only on the parts of the body which are most exposed to the sun’s radiation. Cancerous growths can appear on the inner side of the thighs, on the buttocks, on the genitals and on the soles of the feet even though they are usually found on the back and the front part of the legs. When you perform a self-exam, you must check every inch of your body.

Malignant growths resemble closely common moles.

This is the main reason why they may go unnoticed for a fairly long time. You should keep a close eye on your skin and on any new growths, especially if they develop quickly. You must get frequent mole checks performed by a dermatologist as well.

Take all necessary measures to lower your risk of melanoma.

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3 Of the Leading Causes of Skin Cancer

Skin cancer is one of the commonest forms of this malignant disease. It is commonly caused by exposure of the skin to the sun. Before we talk about the 3 leading causes of skin cancer, let’s take a look at the different types of skin cells and their basic functions. The top layer of the skin is called epidermis, and it has 3 major types of cells squamous, basal and melanocytes. Squamous cells line the inside of the skin, just below the visible outer layer. Below the layer of squamous cells are basal cells, which act as generators of new cells. The final layer of the epidermis consists of melanocytes. These cells produce melanin, a coloring pigment that determines your skin tone. This pigment also plays a vital role in protecting the skin from the harmful UV rays.

1. UV Radiations

A major cause of skin cancer is the ultra violet radiations from the sun. It is caused either due to long-term or short-term exposure to these harmful rays. The 2 common types of UV rays that affect the skin are UVA and UVB. Both the types of sun rays are known to be cancer causing. How do these rays work on damaging the skin cells? They go straight for the jugular – here, the DNA of the skin cells. Once the cell’s code is damaged, the cells tend to multiply quickly, leading to cancerous growth. It is not just the sun’s UV rays are harmful, even radiations from tanning bed and solarium have been found to be carcinogenic.

2. Chemicals

Many chemicals have also been found to cause non-melanoma cancer. Some of the harmful chemicals are arsenic, shale oil, petroleum products, soot, pitch, nicotine, coal-tar and creosote. People working in chemical factories or leather tanneries may be exposed to one or many of these carcinogenic chemicals. Their work conditions make their skin more vulnerable to the UV rays and to skin cancer.

3. Skin Conditions

Those suffering from skin conditions are prone to this form of cancer as the skin cells are already weak and can be easily affected by the carcinogens. Psoriasis, solar keratosis, Gorlin’s syndrome, Xeroderma pigmentosum and eczema could increase the risk of skin cancer. These skin conditions do not by themselves cause skin cancer, but could hasten the formation of cancerous cells as they weaken the skin cells and reduce their natural ability to repair and renew.

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