Schisandrin B: Ushering in a New Era in UV Protective Skincare


Schisandrin B, a key component of Glissandrin, can protect against solar irradiation-induced oxidative injury in skin tissue and skin cells, according to recent research findings from the laboratory of Dr. Robert Ko at the Hong Kong University of Science and Technology.

As the largest organ in the human body, the skin serves as an effective barrier for protecting against various external threats. This includes exposure to harmful solar irradiation – particularly UV and infrared rays – which research has shown to be a major cause of skin aging. Solar irradiation-induced reactive oxygen species (ROS) generation is responsible for photo-aging, the signs of which include wrinkles, coarse skin texture, and reduced skin resilience. Although human skin tissue possesses non-enzymatic and enzymatic antioxidant defense systems to cope with the increased oxidative stress caused by solar light radiation, long-term exposure or over-exposure to solar light can overwhelm the antioxidant system.

But what if there was a way to enhance the skin’s natural antioxidant defenses to prevent photo-aging entirely? Schisandrin B (Sch B) is able to do just that, ushering in a new era in UV protective skincare.

Schisandrin B is derived from the Schisandra fruit, an herb commonly used in Traditional Chinese Medicine (TCM). This naturally occurring herbal ingredient has been found to produce tissue non-specific protection against oxidative injury by enhancing cellular and mitochondrial glutathione antioxidant status in the heart, liver, kidney, and brain.

Figure 1: Schisandra berry

Recent studies led by Dr. Robert Ko at the Hong Kong University of Science and Technology have shown the promise of Schisandrin B:

• Schisandrin B stimulated both reduced-glutathione and vitamin E levels. These two non-enzymatic antioxidants can remove excess ROS during oxidative stress in a synergistic manner.
• Schisandrin B elevated various enzymes involved in the enzymatic antioxidant defense system, demonstrating that non-enzymatic and enzymatic antioxidant components work together to protect against solar irradiation-induced oxidative injury in skin tissue.

Figure 2: Effects of Sch B pretreatment on solar irradiation-induced cell injury in BJ human fibroblasts

• Schisandrin B suppressed the solar irradiation-induced increases in elastases-type protease activity and matrix-metalloproteinases-1 (MMP-1) expression in skin cells. The degradation of the extracellular matrix (EM) in skin tissue as a result of solar irradiation is of prime concern in skincare. This is one of the major biological events that leads to photo-aging and is mediated by protein-degrading enzymes like elastases-type protease and MMP-1.

Figure 3: Effects of Sch B pretreatment on cellular elastases-type protease activity in solar-irradiated BJ human fibroblasts

Figure 4: Effects of Sch B pretreatment on cellular MMP-1 level in solar-irradiated BJ human fibroblasts

Schisandrin B is a key component of Glissandrin™, a potent anti-aging skincare ingredient that has been the subject of over 100 research papers. In-vivo and in-vitro studies have proven the ability of Glissandrin to reverse mitochondrial decay , the leading cause of aging, and to simultaneously enhance the cell’s natural ability to fight oxidative damage.

Other studies have shown the ability of Schisandrin B to suppress collagenase, an enzyme responsible for the depletion of collagen in skin cells. Research has also been conducted on the compound’s anti-cancer properties, particularly in the skin.

Figure 5: Mitochondria


Given that both spectra of solar light – UV and infrared radiation – are major causes of skin aging, Schisandrin B’s ability to enhance the skin’s antioxidant defenses against harmful solar irradiation, thereby offering the prospect of preventing skin photo-aging, is instigating a new era in skincare.

For more information

More information on Schisandrin B, mitochondrial decay, and theories of aging can be found at these independent websites:

• National Institutes of Health (
• PubMed (
• Natural Standard (

Background and References

Schisandrin B is a key component of Glissandrin™, the proprietary ingredient in Glissandra™ products.

Dr. Robert Ko holds a PhD from the University of British Columbia in Vancouver, Canada. He is currently a Professor in the Division of Life Science at the Hong Kong University of Science and Technology, and Chief Technology Officer of Glissandra Skincare Inc.

The Hong Kong University of Science and Technology is ranked 41st among research universities worldwide by Times Higher Education 2010 (London, UK).

Lam PY, Leong PK, Chen N, Ko KM: Schisandrin B enhances the glutathione redox cycling and protects against oxidant injury in different types of cultured cells. Biofactors (in press).

Chiu, P.Y., and Ko, K.M. (2006). Schisandrin B-induced increase in cellular glutathione level and protection against oxidant injury are mediated by the enhancement of glutathione synthesis and regeneration in AML12 and H9c2 cells. Biofactors 26: 221-230.

Chiu, P.Y., Leung, H.Y., and Ko, K.M. (2008). Schisandrin B enhances renal mitochondrial antioxidant status, functional and structural integrity, and protects against gentamicin-induced nephrotoxicity in rats. Biol. Pharm. Bull. 31: 602-605.

Chen, N., Chiu, P.Y., and Ko, K.M. (2008). Schisandrin B enhances cerebral mitochondrial antioxidant status and structural integrity, and protects against cerebral ischemia/reperfusion injury in rats. Biol. Pharm. Bull. 31: 1387-1391.

Lam PY, Yan CW, Chiu PY, Leung HY, Ko KM. Schisandrin B protects against solar irradiation-induced oxidative stress in rat skin tissue. Fitoterapia 2011; 82: 393-400.

Chiu PY, PY Lam, Yan CW, Ko KM. Schisandrin B protects against solar irradiation-induced oxidative injury in BJ human fibroblasts. Fitoterapia 2011; 82: 682-691.

Nisida H, Tatewaki N, Magara T, Nakajima Y, Ko KM, Hamamori Y, Konishi T: Inhibition of ATR kinase activity by schisandrin B in DNA damage response. Nucleic Acid Res. 2009; 37: 5678-5689.

What causes skin aging: Making sense of the latest research findings


This is Part 1 of a 3-part series on the quest by scientists to find effective ways to fight skin aging. By understanding the leading cause of aging, mitochondrial decay, we can develop comprehensive solutions for long-term skin health.

Theories of aging

Aging is a consequence of changes that are harmful, progressive, and thus far irreversible in most living organisms, including humans. Age-associated damage occurs to biomolecules, cells, and organs. Diseases such as arthritis, osteoporosis, heart diseases, cancer, Parkinson’s disease, and Alzheimer’s disease occur more frequently with old age.

The biochemical mechanism of aging has long been an area of intensive research, and a number of theories of aging have been proposed, including the neuro-endocrine theory, which links aging to hormonal changes; immunological theory, which attributes aging to immune system dysfunction; telomerase theory, which relates to the shortening of chromosomes during cell division; and oxidative stress theory, which refers to free radical damage to cells.

Among these theories, it is reasonable to distinguish those that attempt to establish primary causes of aging from those that are secondary. For example, the telomerase theory may be secondary since the decrease in telomerase activity can be caused by the increase in cellular oxidative stress.

In gerontology, the study of aging, oxidative stress is increasingly recognized as the primary cause of aging.

The role of mitochondrial decay in aging

If oxidative stress is indeed the primary factor in skin aging, it is important to understand its roots. Scientists now believe that oxidative stress may be caused by mitochondrial decay. Mitochondria, the chief producers of both energy and oxidants inside the cell, play a critical role in the process of aging.

As energy producers, mitochondria convert unusable forms of energy into a usable chemical form known as adenosine triphosphate (ATP), which is required for all vital cellular chemical reactions throughout the body. During the metabolic cycle of ATP production, oxidants are released from the mitochondria as harmful by-products that can damage important biomolecules, such as DNA, lipids, and proteins. At the same time, the mitochondria themselves are also victims of this metabolic cycle of ATP production as they are highly susceptible to damage by the oxidants thus released.

Over time, largely due to cumulated damage by the oxidants, the functional capabilities of mitochondria deteriorate; the production of ATP declines; and the release of oxidants increases. The latter inflicts greater damage to the mitochondria, which in turn results in accelerated oxidant production. This is the vicious cycle of mitochondrial decay. If left unchecked, mitochondrial decay leads to cumulative damage in cellular biomolecules, resulting in a host of age-related diseases.

Effects of mitochondrial decay on the skin

The skin is the body’s largest organ. The consequence of cumulative damage in skin cell biomolecules is a corresponding increase in the depletion of important extracellular components, such as collagen, elastin, and hyaluronic acid, among others. The loss of these significant components is manifested in the appearance of wrinkles, fine lines, droopiness, pigmentation, puffiness, skin inelasticity, enlarged pores, dryness, and a dull skin tone.


An increasing amount of scientific evidence confirms that mitochondrial decay is the fundamental cause of aging; therefore, scientists are endeavoring to find remedies to reverse the declining functional capabilities of mitochondria due to aging. In Parts 2 and 3 of this series, we will explore what scientists have accomplished in this direction.

More information on mitochondrial decay and theories of aging can be found at these independent websites: