Abstract: As skin ages it deprives its charming youthful expression. Aging may be simple chronological passing of the years or photoaging induced by exposure to the sun. The free radical fabricated in the body commenced response of receptors of nuclear signaling, mitochondrial damage, protein oxidation, telomere based DNA damage, genetic mutations and decrease of many hormone levels. Due to this aging skin displays variable epidermal thickness, dermal elastosis, reduced collagen, increased matrix degrading metalloproteinases, severe atrophy, telangiectases, inflammatory infiltrates and vessel ectasia. The secondary metabolites such as quercetin, polyphenol, flavonoid and flavonol, ellagic acids are obtained from plant extracts, provokes the free-radical scavenging activity, antagonize the UV signaling pathway, inhibition of elastase activity and matrix metalloproteinase expression and increase of expression of procollagen type I. Herbal cosmetics play a leading role in impeding and reversing aging of skin. The botanical ingredients present in herbal cosmetic impact biological functions of skin and contribute nutrients required for the healthy skin. The imperative efforts are constrained to associate the medicinal plants with possible mechanism based on scientifically validated, leading to the emergence of novel cosmeceuticals for prevention of sagging. The information of present review assists the cosmetics scholar for development of novel herbal antiaging formulation producing the reduction of wrinkles, redness and abnormal discolorations that result from aging. The combination of listed medicinal plant can be produced immensely efficient, low toxicity and cost impressive product compared to synthetic antiaging formulation. This review can put forward revolt in the field of cosmetic market.
INTRODUCTION
Skin forms a remarkable protective barrier against the external environment (Costin and Hearing, 2007), helping to regulate temperature and fluid balance, keeping out harmful microbes and chemicals and offering some protection against sunlight (Svobodova et al., 2006; Palm and O’Donoghue, 2007; Hussein, 2005). Due to external and internal causes, the collagen fibers and elastic fibers present in dermal tissue of the skin is modified or damaged which leads to wrinkles formation and sagging on the skin because the elasticity of the skin is reduced, it is one of the measure causes for the skin aging (Kuno and Matsumoto, 2004).
There are two distinct types of skin aging, one of the aging caused due to the passage of time or by the inherited gene is called chronological or intrinsic (internal aging). The chronological aging is regulated mainly by androgens and other hormones. The other type of aging is known as photoaging or extrinsic (external) aging and is caused by environmental factors, such as exposure to the sun’s rays, repetitive facial expressions, gravity, sleeping positions and smoking (Mukherjee et al., 2011). Almost 90% of skin changes due to chronic sun exposure (Zouboulis and Boschnakow, 2001). Extrinsic aging is caused by chronic exposure to UV light so it is also known as photo aging.
MECHANISM OF SKIN AGING
Extrinsic skin aging: Extrinsic skin aging is a collective process and depends mostly on the degree of sun exposure and skin pigment. With chronic skin exposure to UV rays, the stratum corneum thickens, the epidermis becomes acanthotic and there is progressive dysplasia with cellular atypia and anaplasia, reduction in collagen and degeneration of elastic fibers (Yaar and Gilchrest, 2007). The following aspects are integrated with photodamaged aging.
Membrane/nuclear signaling: UV irradiation provokes Reactive Oxygen Species (ROS) which repress the activity of enzyme protein-tyrosine phosphatase κ. This enzyme maintains cell-surface receptors of skin, including receptors for Epidermal Growth Factor (EGF), interleukin (IL)-1, keratinocyte growth factor and Tumour Necrosis Factor (TNF)-α in an inactive (hypophosphorylated) state (Xu et al., 2006). Activated receptors impel to intracellular signaling through stimulation of the stress-associated Mitogen-activated Protein (MAP) kinases p38 and c-Jun amino terminal kinase (JNK) (Fisher et al., 1998). Kinase activation induces the transcription of the nuclear transcription complex AP-1(composed of the proteins c-Jun and c-Fos) (Fisher et al., 2002). Moreover, singlet oxygen breaks lipid membrane resulting to activation of AP-1 through ceramide release and leads to the formation of carbonyl groups (C = O) and accumulation of oxidized damaged dermal proteins. Arachidonic acid unleashed by oxidized membrane lipids is turned by cyclooxygenase enzymes into prostaglandins recruiting inflammatory cells to the area (Yaar and Gilchrest, 2007).
AP-1 increases transcription of MMPs (matrix metalloproteinase) and decreases expression of the procollagen I and III genes and TGF-β (transforming growth factor-β) receptors, with a final outcome of reduced dermal matrix formation and Hence, it reduces the synthesis of collegen (Fisher et al., 2000).
UV-induced collagen degradation is generally incomplete, leading to the agglomeration of partially depraved collagen fragments in the dermis and these are conceived to reduce the structural integrity of the skin. UV also stimulates the Nuclear Factor (NF) κB transcription factor and through neutrophil recruitment and MMP-8 release further intensifies matrix degradation. The disabled proteins incorporating carbonyl groups assemble in the upper portions of the dermis. In addition, mitochondria betray large DNA deletions and compromised function (Yaar and Gilchrest, 2007).
Mitochondrial damage: Mitochondria are cellular organelles that generate energy (ATP) by compelling oxygen. UV effect on the mitochondria electron transport chain produces abundant ROS that can damage mitochondrial DNA (mtDNA). The mitochondrial genome encodes 13 components of the electron transport chain (Graeber et al., 1998) and oxidative damage may be foremost to deletions or rearrangements of the DNA, most likely due to double-strand breaks (Prado et al., 2003; Srivastava and Moraes, 2005) which may affect mitochondrial ability to generate energy for the cell. It is inferred that the consequent decrease in mitochondrial function in photodamaged skin leads to additional accumulation of ROS and further compromises the cell's ability to initiate energy.
Protein oxidation: Oxidative damage can also affect proteins and photodamaged skin exhibits accumulation of ROS-induced devastation in upper dermal proteins (Sander et al., 2002). Oxidative protein impair may result in loss or gain of activity (i.e., enzymes), loss of structural protein function and increased/decreased susceptibility to degradation (Shacter, 2000). While epidermal proteins are routinely hastily degraded by epidermal methionine sulfoxide reductases, oxidized dermal proteins persist longer (Garmyn and Yarosh, 2006).
Telomeres: Telomeres are tandem repeats of a short sequence TTAGGG. It exists in a loop configuration. Telomeres become critically short when these loop is disrupted by cell division or UV irradiation. During cell division telomeres cap (the terminal portion of chromosomes, preventing the fusion of telomeres with each other.) cannot be replicated, so the bases of the telomeres caps are lost with each cell division and finally enters a state of senescence or apoptosis (Blackburn, 2001). When telomeres are damaged by UV irradiation the loops configuration becomes disclosed and through interaction with the Werner protein activates the tumour suppressor protein p53 and other proteins which responsible for DNA damage and also induces senescence or apoptosis (Yaar and Gilchrest, 2007).
Intrinsic skin aging: Intrinsic skin aging also known as natural aging mostly found in sunprotected area. Basically the molecular mechanisms of both the type of skin aging (extrinsic and intrinsic) are similar, for example shortening of telomeres, mutations of mitochondrial DNA, oxidative stress genetic mutations and decrease of many hormone levels. According to the free-radical theory of aging, ROS, chiefly commencing from oxidative cell metabolism, play a notable role in both chronological aging and photoaging (Fisher et al., 2002). In spite of several antioxidative mechanisms, which decline with increasing age, abound with ROS damage composed of cell's components. This damage induces to increasing ROS and decreasing antioxidative capacities and finally to cellular aging (Makrantonak and Zouboulis, 2007). ROS influence the transcription factor c-Jun via MAPK (mitogen-activated protein kinases) in extrinsic and intrinsic skin aging. This induction triggers transcription factor called activator protein 1(AP-1), which leads to the expression of matrix metalloproteinases MMP-1 (interstitial collagenase), MMP-3 (stromelysin 1) and MMP-9 (gelatinase b) (Chung et al., 2000). In tendering with these outcomes elevated levels of partially degraded collagen are present in intrinsically aged skin similar to photoaged skin. In intrinsically aged skin expression of the Connective Tissue Growth Factor (CTGF) and Transforming Growth Factor (TGF)-β/Smad signalling are reduced due to which expression of type I procollagen also become less (Quan et al., 2009; Kohl et al., 2011).
Hormonal changes can also alter intrinsic skin aging. The exhibition of sex hormones in the gonads, the pituitary and adrenal glands already gradually decline in the mid-twenties. The hormone oestrogens and progesterone start dwindling during menopause. In particular, the imperfection in oestrogens and androgens cause dryness, wrinkling, epidermal atrophy, collagen breakdown and loss of elasticity (Kohl et al., 2011).
HERBAL COSMETIC PREVENTING SKIN AGING
Herbal cosmetics play a leading role in impeding and reversing aging of skin. Ingredients present in herbal cosmetic impact biological functions of skin and it also provide required nutrition for the healthy skin. The application of herbal antiaging products has been proliferated to many folds in personal-care practice and over, there is a noteworthy demand for the herbal cosmetics. All this occurred due to the extravagant use of synthetic based products in the last one and half century; their production and usage cause human health imperiled with several adverse effects leading to innumerable. It also incited substantial pollution and disturbed our eco-system. Now a day Personal care industry is more focalize on herbal based cosmetics as it is a fast growing segment in the world. Herbal cosmetics are not pondered under the preview of Drugs and Regulations of Food and Drug Administration’s (Kapoor, 2005). The imperative efforts are constrained to associate the medicinal plants with possible mechanism based on scientifically validated, leading towards the emergence of novel cosmeceuticals for prevention of sagging. Medicinal plants restraining skin aging are listed in Table 1.
DISCUSSION
In the field of cosmetic antiaging are mostly demarcated as an agent who preventing and eliminating the wrinkles and sags of the skin (Kuno and Matsumoto, 2004). Over the years, many various compounds and formulations have been used in eradication of skin aging (Farooqi et al., 2002).
The compositions of synthetic antiaging formulations include ingredients that are not always eco-friendly and are for that reason economically unviable. Some of the prior art antiaging formulations also contain components that are ultimately harmful to the skin (Farooqi et al., 2002). The natural skin-care products are quickly absorbed by the superficial layers in the skin and are hypo-allergenic in nature. However, the active ingredients of synthetic skin care product produce an adverse effect on skin such as allergic contact dermatitis, irritant contact dermatitis, phototoxic and photo-allergic reactions (Mukherjee et al., 2011). Additionally, the natural herbs have despicable mammalian toxicity and can be handled safely. This makes the use of natural formulation by manufacture of skin-care products attractive and is becoming common (Farooqi et al., 2002). Manifold herbs, notably fruits, vegetables and whole grains comprise antioxidants, polyphenols scavenging free radicals and eradicate byproducts of metabolism. Today, herbal cosmetics are in demand in whole world due to its significant impact on skin aging.
The over exposure of UV radiation to skin cause's DNA damage and reducing cellular DNA repair capacity, are sources of photoaging. It has been proclaimed that paeoniflorin obtained from Paeonia lactiflora produces protective effects on UV-induced DNA damage (Lee et al., 2006a). This suggests that topical application of Paeoniae lactiflora extracts could improve the ability of the skin to repair DNA damage and prevent from photoaging.
The anthocyanins like cyanidin-3-glucoside, petunidin-3-glucoside, malvidin-3-glucoside and delphinidin-3-glucoside obtained from the berries of Vaccinium uliginosum diminished UV-induced augmented-release of IL-6 and IL-8 by suppressing the function of enzyme protein-tyrosine phosphatase κ. The inhibition of secretion of IL may validate to be a worthwhile means to achieve protection against UV irradiation.
| Table 1: | List of antiaging plants manifests chemical constituents and possible mechanism of action |
Botanical antioxidants have been notified to have a good potential as antiaging agents. For example, dietary grape seed proanthocyanidins arose in inhibition of the expressions of Proliferating Cell Nuclear Antigen (PCNA) and cyclooxygenase-2 (COX-2) in the skin. Flavonoids are the largest group among plants with active properties; more than, 5000 flavonoids have been extracted and identified (Chiu et al., 2009), decrease the early activation of signaling pathway in response to UV induced injury.
The quercetin, polyphenol, flavonoid and flavonol, ellagic acids are obtained from natural resources, produces the free radical scavenging activity, inhibition of elastase activity and MMP expression and increase of expression of procollagen type I (Kim et al., 2007a, 2008a; Maity et al., 2011; Moon et al., 2005). Moreover, active constituents having antioxidant properties obtained from plant extracts, inhibit elastase, hyaluronidase, collagen synthesis, lipid peroxidation activity, protein expression of procollagen and prevent MMP gene induction and due to this fibrillin fibre length elongated to maintain elasticity of skin (Satardekar and Deodhar, 2010; Aslam et al., 2006). The above characters of ingredients help to minimize the environmental effects and stress to the skin. Moreover, it also improve texture, firmness and elasticity, counteract dryness, smooth out wrinkles, minimize age spots, improve color and increase moisture content of the skin.
CONCLUSION
Skin aging may be categorized as intrinsic and extrinsic. The anti-aging cream must include a unique composition with DNA repair and cellular repair molecules. The bioactive components such as flavonoids, polyphenols, tannins, quercetin etc from a variety of plant sources are combined actively to reduce wrinkles, reverse sun damage, diminish redness and abnormal pigment and improve the signs in the various categories of skin aging. The information of present review assists the cosmetics scientists for development of novel herbal antiaging formulation producing the reduction of wrinkles, redness and abnormal discolorations that result from aging. The combination of listed medicinal plant can be produced immensely efficient, low toxicity and cost impressive product compared to synthetic antiaging formulation.
The provision of such high-pitched information will authenticate the scholar for further development of herbal cosmetic, in order that more societal people can benefit from a more widely available, safer and more certified practice of herbal cosmetics in the future. This review can put forward revolt in the field of cosmetic market.
ACKNOWLEDGMENT
Authors pay indebtedness to Columbia Institute of Pharmacy, Raipur for providing library and online journal facilities.