The anti-melanogenic effect of pycnogenol by its anti-oxidative actions

Kim, You Jung; Kang, Ki Sung; Yokozawa, Takako

doi:10.1016/j.fct.2008.04.002

Cited by 116 publications

(84 citation statements)

References 37 publications

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“…6) We have reported on the significance of maintaining cellular redox through the down-regulation of RS and the boosting of antioxidant defenses in the inhibition of melanogenesis. 5,7,8) Various phenolic compounds from natural sources have been reported as melanogenic inhibitors. 5,[7][8][9][10][11] Hyperin and quercetin are two phenolic flavonoids reported to have antioxidative 12) and anti-viral 13) properties.…”

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confidence: 99%

Hyperin and Quercetin Modulate Oxidative Stress-Induced Melanogenesis

Kim

2012

Biological & Pharmaceutical Bulletin

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Hyperin and quercetin are phenolic compounds present in fruits and vegetables that have been reported to possess strong anti-oxidative properties. Although increasing evidence strongly suggests that antioxidants suppress the melanin synthesis that is causally associated with oxidative stress, the protective actions of hyperin and quercetin against oxidative stress-induced melanogenesis have not been fully explored. To elucidate the suppressive effects of hyperin and quercetin on oxidative stress and melanin synthesis, peroxynitrite (ONOO ) scavenging activity was measured in vitro as were quantifications of melanin content, intracellular total RS, ONOO , superoxide (• O 2 ), nitric oxide (NO • ), catalase activity and the reduced glutathione (GSH)/ oxidized glutathione (GSSG) ratio. Results showed that in vitro, hyperin and quercetin reduced ONOO . Additionally, hyperin and quercetin suppressed total RS, ONOO ,• O 2 , and NO• , catalase activity, and melanin synthesis, while they boosted the GSH/GSSG ratio in B16F10 melanoma cells (B16 cells). Therefore, I propose that hyperin and quercetin have a powerful capacity to modulate oxidative stress-induced melanogenesis.Key words hyperin; quercetin; antioxidant; oxidative stress; melanogenesis Melanogenesis is the process by which pigment forms and melanin is synthesized in special organelles called melanosomes.1) Melanin plays a key role in the protection of the skin against deleterious sunlight under normal conditions, but also can increase the generation and excessive accumulation of melanin that lead to clinical and cosmetic concerns such as freckles, age spots, sites of actinic damage, and melasma. Chronic inflammation, UV ray radiation, and the release of abnormal α-melanocyte stimulating hormone (α-MSH) also are well-known triggering factors for abnormal melanogenesis and inflammatory pigmentation. 1,2)Oxidative stress caused by excessive reactive species (RS), including reactive oxygen species (ROS) and reactive nitrogen species (RNS), is known to be associated with skin aging and hyperpigmentation. Also, a deficient anti-oxidative defense system, such as a disturbed redox balance and weak anti-oxidant enzyme activity, exacerbate skin aging and hyperpigmentaion.3-5) Therefore, searching for natural antioxidants that inhibit melanogenesis has been an important strategy in the development of skin medications and cosmetics. 6) We have reported on the significance of maintaining cellular redox through the down-regulation of RS and the boosting of antioxidant defenses in the inhibition of melanogenesis. 5,7,8) Various phenolic compounds from natural sources have been reported as melanogenic inhibitors. 5,7-11) Hyperin and quercetin are two phenolic flavonoids reported to have antioxidative 12) and anti-viral 13) properties. However, the effects of hyperin and quercetin on oxidative stress-induced melanogenesis have not been fully explored to date.To estimate the effects of hyperin and quercetin on oxidative insult in vitro, peroxynitrite (ONOO − ) scavenging act...

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confidence: 99%

Hyperin and Quercetin Modulate Oxidative Stress-Induced Melanogenesis

Kim

2012

Biological & Pharmaceutical Bulletin

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“…Vitamin C has various metabolic activities such as an antioxidant capacity that can protect cells from oxidative stress (20,34). An antioxidative property may be defined as a capacity for the scavenging of free radicals including ROS and reactive nitrogen species by donating a hydrogen or an electron (35). There have been many reports of the therapeutic or preventive efficacy of vitamin C as an anticancer agent (36,37), but no study of the DENinduced HCC model has been conducted using congenital vitamin C-deficient Smp30 KO mice.…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of Vitamin C on Diethylnitrosamine-induced Hepatotoxicity in Smp30 Knockout Mice

Son

Ullah

Elfadl

et al. 2018

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Abstract. Vitamin C (L-ascorbic Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death, resulting in approximately 0.7 million deaths each year, and the sixth most common malignancy worldwide (1-3). The recognized risk factors for HCC are hepatic disorder associated with steatosis, cirrhosis, viral hepatitis, alcohol, chemical agents, obesity, metabolic syndrome, and so forth (4). Despite recent advances in diagnosis and treatment, the effectiveness of therapy for HCC remains unsatisfactory, and HCC has a hidden development and a poor prognosis (5, 6). Therefore, there is an urgent requirement for novel therapeutic compounds for the treatment of patients with HCC. Many animal models of hepatocarcinogenesis have been established to examine the effects of therapeutic agents. Diethylnitrosamine (DEN) is frequently used as a hepatocarcinogenic agent in rodents (1). In our experimental model, externally visible foci were observed and measured by stereomicroscopy. It has been established that DEN induces HCC in animals with a developmental course similar to that of human HCC (7). Furthermore, DEN is an indirect alkylating agent that induces the generation of reactive oxygen species (ROS), which damage DNA through oxidation (8).Senescence marker protein-30 (SMP30) is a calciumbinding protein, and its levels in the liver, kidney, and lung become significantly down-regulated with aging in an androgen-independent manner (9, 10). SMP30 plays an important role in calcium (Ca 2+ ) homeostasis (11). Ca 2+ is one of the most universal and physiologically significant signaling molecules that especially affects cell apoptosis and cell necrosis (12). Other reports have indicated that SMP30 participates in controlling the activity of antioxidant enzymes 93

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“…RS is major and significant contributors to skin hyperpigmentation and skin aging [15]. It has generally been believed that agents that have antioxidant activity show anti-aging, whitening, and anti-inflammatory activities [16].…”

Section: Discussionmentioning

confidence: 99%