Background: Morin is a family of phenolic compounds and is a bioflavonoid ingredient in fruits and vegetables. Morin exhibits various biological activities, including antioxidant cell protection and antimutagenic and anti-inflammatory effects; these activities safely minimize free radical-mediated damage biologically. However, the photoaging mitigation effect of morin on skin cells remains unknown. To investigate the effect of the morin on cell senescence mitigated against photoaging, cell viability, antioxidation, and anti-inflammation experiments were conducted. As a natural result of oxygen consumption, reactive oxygen species (ROS) in the form of harmful superoxides and hydroxyl radicals are generated through an oxidation reaction involving heavy metal cations such as iron. This adversely affects DNA, lipids, and proteins; therefore, organisms have a self-protective mechanism against oxidative stress via enzymes such as catalase (CAT) and superoxide dismutase (SOD), molecules such as glutathione, and proteins such as thioredoxin. Therefore, in this study, the antioxidative and skin protection functions of morin were examined to investigate the possibility of cosmetics. Methods: To examine morin-mediated anti-photoaging mechanisms, human dermal fibroblasts (HDFs) were selected as the model cell line and UVA was selected as the stimulus source. The water-soluble tetrazolium salt-1 assay was performed to assess cell viability and cytoxicity in UV-exposed HDFs. To examine the molecular mechanism underlying the antioxidation capacity of morin, genes were analyzed using qRT-PCR, the expressions of several antioxidant enzymes were monitored, and the effect of morin on GPx1, CAT, HO-1, and NRF2 expressions in UV-exposed HDFs was assessed. Results: The results of the morin toxicity showed the cell viability was above 100% when the concentration of morin was set at 20 and 50 μM. The cytotoxicity test for oxidative stress through UVA showed that the appropriate intensity of UVA 10 J/cm 2 was set as the cell viability reduced by 10 J/cm 2. And the cell survival over 100% rate after the morin treatment was 20 and 50 μM cell. A result of mRNA experiments verified that the expression of the antioxidant enzyme genes GPx1, CAT, HO-1, and NRF2 increased with morin, in a concentration-dependent manner. Conclusion: Morin increases the expression of antioxidant enzymes, which facilitates the antioxidant mechanism to respond to oxidative stress associated with exposure to UV and heat, which are considered to be the most harmful factors damaging the skin cells. This results in ROS removal, a byproduct of the natural metabolism of oxygen and the protection of neurons and proteins from toxicity. In conclusion, this study verified the applicability of morin as a cosmetic ingredient for the protection of cells against oxidization and UV.
Background: Embelin is a major active ingredient of Embelia ribes Burm. belonging to Myrsinaceae, an important traditional medicinal plant of Indian origin. Embelin has a benzoquinone derivative structure and has been studied for anticancer, anti-inflammatory, and antioxidative effects. However, there have been no studies on the use of cosmetic raw materials for embelin. In this study, antioxidant and inhibition of senescence effects of embelin were examined using hydrogen peroxide (H 2 O 2)-induced cellular aging model of human dermal fibroblast. Methods: Cell viability was measured using the principle of water-soluble tetrazolium salt (WST-1) assay. qRT-PCR was used to quantitatively analyze gene expression patterns in human dermal fibroblasts (HDFs) by embelin. Dichlorofluorescein diacetate (DCF-DA) was used to measure changes in intracellular reactive oxygen species (ROS) concentration. Cell senescence was measured using the senescence-associated β-galactosidase (SA-β-galactosidase) assay, a method of staining β-galactosidase. A wound healing assay was used to observe cell mobility. Results: The WST-1 assay demonstrated that decreased cell viability by H 2 O 2 was restored by embelin in a dose-dependent manner. In addition, the expression of SOD1, GPx1, and CAT genes were upregulated by embelin suggesting that embelin-induced antioxidant capability may be enhanced through the upregulation of intracellular antioxidant-related genes. To determine whether embelin inhibits cell senescence in H 2 O 2-induced senescence model of HDFs, the SA-β-galactosidase assay was performed. Embelin decreased the SA-β-galactosidase activity in a dose-dependent manner in H 2 O 2-treated HDFs. Moreover, the expression of p21 and MMP1 genes were reduced by embelin in H 2 O 2-treated HDFs in a dose-dependent manner. However, COL1A1 genes were increased by embelin in H 2 O 2-treated HDFs in a dose-dependent manner. Conclusions: These results suggest that embelin has a potential as an antiaging cosmetic ingredient with antioxidant and anti-senescence properties.
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