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Korean Journal of Medicinal Crop Science - Vol. 33, No. 6
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Korean Journal of Medicinal Crop Science - Vol. 33, No. 6, pp.375-382
Abbreviation: Korean J. Medicinal Crop Sci
ISSN: 1225-9306 (Print) 2288-0186 (Online)
Print publication date 30 Dec 2025
Received 06 Nov 2025 Revised 15 Dec 2025 Accepted 16 Dec 2025
DOI: https://doi.org/10.7783/KJMCS.2025.33.6.375

Sesamin from Artemisia littoricola Attenuates UVA-Induced MMP Expression in Human Dermal Fibroblasts via MAPK Pathway Modulation
Fatih Karadeniz1 ㆍ Chang-Suk Kong2, 3 ㆍ Youngwan Seo4 ㆍ Jung Hwan Oh5, 6, †
1Associate professor, Marine Biotechnology Center for Pharmaceuticals and Foods, College of Medical and Life Sciences, Silla University, Busan 46958, Korea
2Director, Marine Biotechnology Center for Pharmaceuticals and Foods, College of Medical and Life Sciences, Silla University, Busan 46958, Korea
3Professor, Department of Food and Nutrition, College of Medical and Life Sciences, Silla University, Busan 46958, Korea
4Professor, Division of Convergence on Marine Science, College of Ocean Science and Technology, Korea Maritime and Ocean University, Busan 49112, Korea
5Assistant professor, Marine Biotechnology Center for Pharmaceuticals and Foods, College of Medical and Life Sciences, Silla University, Busan 46958, Korea
6Assistant professor, Nutritional Education, Graduate School of Education, Silla University, Busan 46958, Korea

UVA 조사된 인체피부섬유아세포에서 갯제비쑥에서 분리한 sesamin의 MAPK 경로 조절을 통한 MMP의 발현 억제효과
카라데니즈 파티1 ㆍ 공창숙2, 3 ㆍ 서영완4 ㆍ 오정환5, 6, †
1신라대학교 해양식의양소재융합기술연구소 조교수
2신라대학교 해양식의양소재융합기술연구소 소장
3신라대학교 식품영양과 교수
4국립한국해양대학교 해양과학융합학부 교수
5신라대학교 해양식의약소재융합기술연구소 조교수
6신라대학교 교육대학원 영양교육전공 조교수
Correspondence to : †+82-51-999-5796 (E-mail) jhoh@silla.ac.kr


This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Funding Information ▼
ABSTRACT
Background

Photoaging is predominantly caused by ultraviolet (UV) radiation and is a major contributor to premature skin aging. Photoaging of the skin is characterized by oxidative stress and collagen degradation. Damage to skin extracellular matrix proteins is mainly caused by the upregulation of matrix metalloproteinases (MMPs). Sesamin, a lignan commonly found in sesame seeds, possesses antioxidant, anti-inflammatory, and other beneficial properties, making it a promising compound for skin photoprotection.

Methods and Results

The photoaging amelioration potential of sesamin isolated from Artemisia littoricola was investigated using UVA-stimulated human dermal fibroblasts (HDFs). Sesamin significantly reduced intracellular ROS accumulation and attenuated UVA-mediated elevation in secreted MMP-1. Sesamin also suppressed phosphorylation of the terminal mitogen-activated protein kinases (MAPKs), ERK, JNK, and p38. MMP-1 and MMP-3 protein levels were also downregulated, and collagen content was preserved.

Conclusions

These results demonstrate that sesamin protects against UVA-induced damage in HDFs by reducing oxidative stress and inhibiting MAPK-mediated MMP expression. These results indicate that sesamin is a potential natural photoprotective agent with potential applications in skin care. Isolation of sesamin from A. littoricola highlights the relevance of medicinal crops as a source of bioactive compounds for cosmeceutical applications.

KeyWords: Artemisia littoricola, Human Dermal Fibroblasts, Matrix Metalloproteinases-1, Photoaging, Sesamin
INTRODUCTION

Skin photoaging is a multifactorial process characterized by the excessive degradation of collagen fibers and the consequent remodeling of the extracellular matrix (ECM). These processes lead to wrinkles, loss of elasticity and strength, impaired skin repair and other signs of premature skin aging. Ultraviolet (UV) radiation which penetrates the dermis is the most important environmental factor behind these detrimental changes. Among other types of UV, UVA penetrates deeper into skin and UVA exposure induces the overgeneration of reactive oxygen species (ROS) which in turn activates matrix metalloproteinases (MMPs), particularly MMP-1, MMP-3 and MMP-9 enzymes which are responsible for collagen degradation and ECM disruption (Gromkowska-Kępka et al., 2021). The accumulation of ROS is also known to trigger intracellular signaling cascades, including the mitogen-activated protein kinase (MAPK) pathway which enhances MMP expression and contributes to inflammatory responses and detrimental effects (Prasanth et al., 2020).

Given the pivotal role of oxidative stress in photoaging, natural compounds with antioxidant and MMP-inhibitory activities have gained considerable attention as potential photoprotective agents. Plant-derived bioactive compounds, including polyphenols, flavonoids and lignans have been studied for their ability to mitigate UVA-induced damage via antioxidant properties, suggesting a promising strategy for preventing or attenuating photoaging (Calvo et al., 2024; Lin et al., 2024). Some studies have demonstrated that compounds like caffeic acid phenethyl ester and ferulic acid possess antioxidant properties and can inhibit MMP expression, thereby protecting the skin from UV-induced damage (Staniforth et al., 2012; Shin et al., 2019).

Sesamin, a major lignan found in sesame seeds (Sesamum indicum) and several other plant species, exhibits a broad spectrum of biological activities including but not limited to antioxidants, anti-inflammatory and anti-cancer effects (Wu et al., 2019; Zhang et al., 2022). Its antioxidant properties allow it to scavenge ROS, modulate redox sensitive signaling pathways and suppress oxidative damage while its anti-inflammatory activity may reduce the production of pro-inflammatory cytokines associated with skin aging. Previous studies have demonstrated its protective effects in various cell and animal models, but its potential as a photoprotective agent against UVA-induced skin damage remains underexplored.

Sesamin was isolated for the first time from Artemisia littoricola in the present study. A. littoricola is a medicinal plant and it is known for its diverse bioactive compounds (Kwon and Lee, 2001). The current study focused on the ability of sesamin to attenuate deteriorative effects of UVA exposure via reducing oxidative stress, regulating MMP secretion and controlling key signaling pathways, particularly the MAPK cascade which was aimed at providing mechanistic insights into its potential action mechanism as a natural anti-photoaging agent.

MATERIAL AND METHODS
1. Chemicals and reagents

Sesamin (Fig. 1A) was isolated from Artemisia littoricola and identified by comparison of its 1H and 13C NMR data with reported literature (Baures et al., 1992). Dulbecco's modified Eagle's medium (DMEM), fetal bovine serum (FBS) and penicillin-streptomycin were purchased from Gibco (Thermo Fisher Scientific, Waltham, MA, USA). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 2',7'-dichlorofluorescin diacetate (DCFH-DA), and other analytical-grade chemicals were obtained from Sigma-Aldrich (St. Louis, MO, USA). ELISA kits for human MMP-1 were obtained from R&D Systems (Minneapolis, MN, USA). Antibodies against MMP-1, MMP-3, collagen type I, ERK, phospho-ERK, JNK, phospho-JNK, p38, phospho-p38, and β-actin were purchased from Cell Signaling Technology (Danvers, MA, USA). All reagents were of the highest commercial grade available.


Fig. 1.  Sesamin structure and its cytotoxicity profile in HDFs.

(A) Chemical structure of sesamin isolated from A. littoricola derived from 1H and 13C NMR spectra. Spectra confirm characteristic signals of the lignan framework. (B) Cell viability of HDFs treated with increasing concentrations of sesamin (1–50 µM) for 24 h. No significant cytotoxicity was observed. Values are expressed as mean ± SD (n = 3).



2. Cell culture

Human dermal fibroblasts (HDFs; ATCC PCS-201-012) were maintained in DMEM supplemented with 10% (v/v) heat-inactivated FBS, 100 U/mL penicillin and 100 µg/mL streptomycin at 37℃ in a humidified atmosphere containing 5% CO2. Cells were sub-cultured every 23 days using 0.05% trypsin–EDTA and seeded at appropriate densities for each experiment. Cells between passages 5 and 10 were used for all assays.

3. UVA irradiation and sample treatment

For UVA exposure, cells were washed twice with phosphate-buffered saline (PBS, pH 7.4) and covered with a thin layer of PBS to prevent drying. UVA irradiation was performed using a Bio-Sun biological UV–irradiation system (Vilber Lourmat, Marine, France) equipped with 4× 30-Watt 365 nm UVA lamps (T.40L, Vilber Lourmat) at a measured intensity of approximately 6 J/cm2, as calibrated with a UV radiometer (VLX-3W, Vilber Lourmat). After irradiation, PBS was replaced with serum-free DMEM containing sesamin at the indicated concentrations (1–50 µM) and incubated at 37℃. Non-irradiated and untreated cells served as negative controls.

4. Cell viability assay (MTT)

The cytotoxicity of sesamin was determined using the MTT assay as previously described (Oh et al., 2021). HDFs were seeded in 96-well plates at 1 × 104 cells/well and allowed to adhere overnight, and absorbance was measured at 540 nm using a GENios microplate reader (Tecan Austria GmbH, Grodig, Austria). Cells were treated with sesamin (0–50 µM) for 24 h, followed by incubation with MTT (0.5 mg/mL) for 3 h. The formazan crystals formed were dissolved in dimethyl sulfoxide (DMSO) and cell viability was expressed as a percentage of the untreated control.

5. Measurement of intracellular ROS

Intracellular ROS generation was quantified using the DCFH-DA fluorescent probe. After treatment and UVA exposure, cells were incubated with 10 µM DCFH-DA in serum-free medium for 30 min at 37℃. Excess dye was removed by washing with PBS, and fluorescence was measured at excitation/emission wavelengths of 485/530 nm using a microplate reader (GENios, Tecan). Relative ROS levels were calculated as a percentage of the UVA-irradiated control group.

6. Enzyme-linked immunosorbent assay (ELISA)

Secreted MMP-1 levels were determined in cell culture supernatants using a commercial ELISA kit according to the manufacturer’s protocol. Briefly, conditioned media were collected, centrifuged at 10,000 × g for 10 min to remove debris and incubated in antibody-coated wells. Absorbance was read at 450 nm, and MMP-1 concentrations were normalized to total protein content and quantified from standard curves according to manufacturer’s instructions.

7. Semi-quantitative RT-PCR

Total RNA was extracted using TRIzol reagent (Invitrogen, Carlsbad, CA, USA), and 2 µg RNA was reverse-transcribed using M-MLV reverse transcriptase (Promega, Madison, WI, USA). PCR amplification was performed using Luna Universal qPCR Mix (New England Biolabs, Ipswich, MA, USA) with specific primers for MMP-1, MMP-3, COL1A1, and β-actin (internal control) under the following conditions: 95℃ for 5 min, followed by 30 cycles of 95℃ for 45 s, 60℃ for 60 s, and 72℃ for 45 s, with a final extension at 72℃ for 5 min in TP800 Thermal Cycler Dice™ Real Time System (Takara Bio, Ohtsu, Japan).

8. Western blot analysis

Cells were lysed in RIPA buffer containing protease and phosphatase inhibitors (Thermo Fisher Scientific). Equal amounts of protein (20 µg) were separated by SDS-PAGE and transferred to nitrocellulose membranes (Millipore, Billerica, MA, USA) using Trans-Blot Turbo (Bio-Rad, Hercules, CA, USA). Membranes were blocked with 5% skim milk in TBS-T (Tris-buffered saline containing 0.1% Tween-20) for 1 h and incubated overnight at 4℃ with primary antibodies (1:1000). After washing, membranes were incubated with HRP-conjugated secondary antibodies (1:5000) for 1 h. Bands were visualized using an ECL detection kit (Thermo Fisher Scientific) and quantified by densitometry using ImageJ. Protein expression levels were normalized to β-actin.

9. Statistical analysis

All experiments were performed in triplicate (n = 3). Data were expressed as mean ± standard deviation (SD). Statistical analyses were conducted using one-way analysis of variance (ANOVA) followed by Duncan’s multiple range test using SPSS version 25.0 (IBM Corp., Armonk, NY, USA). Differences were considered statistically significant at p < 0.05.

RESULTS
1. Cytotoxicity of sesamin in human dermal fibroblasts

The cytotoxicity of sesamin in human dermal fibroblasts (HDFs) was assessed using the MTT assay following treatment with increasing concentrations of sesamin (0, 1, 5, 10, 25, and 50 µM). Cell viability remained above 90% across all concentrations tested, indicating minimal cytotoxicity under the experimental conditions (Fig. 1B). Notably, treatment with the highest concentration (50 µM) maintained statistically full viability relative to untreated control cells, confirming that sesamin is well-tolerated by HDFs at concentrations used in subsequent experiments.

2. Sesamin reduces UVA-induced intracellular ROS generation

Exposure to UVA irradiation (6 J/cm2) significantly increased intracellular ROS levels in HDFs which were normalized to 100% for easy comparison. Sesamin treatment at concentrations of 25 µM and 50 µM markedly decreased ROS levels to 82.96% and 75.44%, respectively (Fig. 2A). Lower concentrations of sesamin (5 µM) produced only modest reductions that were not statistically significant. The reductions observed at 25 µM and 50 µM were statistically significant at p < 0.01 indicating that sesamin effectively attenuates UVA-induced oxidative stress in HDFs in a dose-dependent manner.


Fig. 2.  Sesamin reduces intracellular ROS generation and MMP-1 secretion in UVA-stimulated HDFs.

(A) Intracellular ROS levels measured by DCFH-DA fluorescence assay in HDFs exposed to UVA (6 J/cm2) and treated with sesamin. (B) ELISA quantification of MMP-1 secretion from HDFs following UVA exposure with or without sesamin treatment. Data are shown as mean ± SD (n = 3). ##p < 0.01 vs. blank group; **p < 0.01 vs. UVA-only control.



3. Inhibition of UVA-induced MMP-1 secretion by sesamin

MMP-1 secretion, evaluated using ELISA, was significantly elevated upon UVA exposure, increasing from 9.58 ng/ml in untreated controls to 14.68 ng/ml. Treatment with sesamin led to a dose-dependent suppression of MMP-1 levels: 5 µM (13.77 ng/ml), 10 µM (13.14 ng/ml), and 50 µM (9.87 ng/ml) (Fig. 2B). The inhibitory effect at 50 µM was statistically significant (p < 0.01), demonstrating that sesamin can effectively counteract UVA-induced MMP-1 overproduction.

4. Modulation of MMP gene expression

Semi-quantitative RT-PCR analysis revealed that UVA irradiation upregulated mRNA levels of MMP-1, MMP-3 and MMP-9 (set as 1.0 in control cells). Treatment with 50 µM sesamin reduced MMP-1 expression to 0.23-fold and MMP-3 to 0.14-fold relative to UVA-only samples (Fig. 3). Although a decrease in MMP-9 expression was observed, it did not reach statistical significance compared to UVA controls. These results suggest that sesamin selectively downregulates MMPs most relevant to ECM degradation during photoaging.


Fig. 3.  Sesamin modulates gene expression of MMPs.

Relative mRNA expression levels of (A) MMP-1, (B) MMP-3, and (C) MMP-9 in UVA-stimulated HDFs as determined by qRT-PCR. Sesamin reduced MMP gene expression β-actin was used as a loading control. Data are shown as mean ± SD (n = 3). #p < 0.05 vs. blank group; * p < 0.05 and **p < 0.01 vs. UVA-only control.



5. Sesamin restores collagen and suppresses MMP protein levels

Western blot analysis confirmed that UVA-induced upregulation of MMP-1 and MMP-3 proteins was significantly reduced following sesamin treatment at 5, 10, and 50 µM (Fig. 4A). Concurrently, collagen I expression, which was suppressed to approximately 82% by UVA irradiation, was partially restored following sesamin treatment. At 50 µM, MMP-1 and MMP-3 protein levels decreased to approximately 42% and 23%, respectively, while collagen I expression recovered to 72% of control levels Fig. 4B. These findings indicate that sesamin protects ECM integrity by suppressing MMP protein expression and preserving collagen content.


Fig. 4.  Sesamin modulates protein expression of MMPs in UVA-stimulated HDFs.

(A) Representative Western blot images of MMP-1, MMP-3 and collagen in UVA-stimulated HDFs with or without sesamin treatment. (B) Densitometric quantification of protein expression levels normalized to β-actin. Data are shown as mean ± SD (n = 3). #p < 0.05 vs. blank group; * p < 0.05 and **p < 0.01 vs. UVA-only control.



6. Inhibition of MAPK signaling by sesamin

UVA irradiation induced phosphorylation of MAPK proteins, including ERK, JNK, and p38, which are key regulators of MMP expression Fig. 5A. Treatment with 50 µM sesamin significantly suppressed phosphorylation levels of ERK, JNK, and p38 by 52%, 49%, and 59%, respectively (Fig. 5B). This result indicates that sesamin’s inhibitory effect on MMP expression may be mediated through modulation of MAPK signaling pathways, contributing to its overall photoprotective effect.


Fig. 5.  Sesamin modulates MAPK pathway phosphorylation in UVA-stimulated HDFs.

(A) Representative Western blot images of phosphorylated ERK (p-ERK), JNK (p-JNK), and p38 (p-p38) in UVA-stimulated HDFs treated with or without sesamin. (B) Densitometric quantification of MAPK phosphorylation levels normalized to β-actin. Data are presented as mean ± SD (n = 3). #p < 0.05 vs. blank control; *p < 0.05 vs. UVA-only control.



DISCUSSION

In this study, sesamin isolated from A. littoricola demonstrated a protective effect against UVA-induced damage in human dermal fibroblasts, as assessed by viability, ROS production, MMP-1 release and expression and MAPK pathway modulation. These findings add to the already present body of knowledge on sesamin and on plant-based anti-photoaging agents using in vitro dermal fibroblast models.

Current results align with prior reports of sesamin’s antioxidative effects. For example, sesamin was shown to reduce intracellular ROS after UVB exposure in Hs68 cells, attenuate and enhance TIMP-1 and thereby increasing total collagen content (Lin et al., 2019). In particular, sesamin reduced iNOS and COX-2 expression, inhibited NF-κB translocation, and prevented epidermal hyperplasia and wrinkle formation in hairless mice after chronic UVB exposure.

More recently, a study by Li et al. (2024) demonstrated that sesamin attenuated UV-induced keratinocyte injury via reducing MMP-1 and MMP-9 in keratinocytes. The mechanistic motif of MAPK modulation (especially JNK/p38) via suppression of phosphorylation appears consistent with other sesamin reports. Thus, current data reinforces and extends these reports by demonstrating that in dermal ECM-relevant cells, sesamin could suppress UVA-induced MMP-1 expression (both secreted and mRNA), reduce ROS and down-modulate phosphorylated ERK, JNK and p38. This suggests that sesamin’s photoprotective effect is present across different skin cell types (keratinocyte, fibroblast) across UV spectra (UVB, UVA).

The present findings strengthen the established photoaging progression in which ultraviolet irradiation elevates intracellular ROS levels, leading to activation of the MAPK family (ERK, JNK, and p38). This canonical signaling pathway is widely accepted as a standard pathway to look into in photoaging research. Accordingly, MAPKs along with their downstream targets MMP-1, MMP-3, and collagen were specifically selected in this study to evaluate the protective mechanism of sesamin against UV-induced skin aging. Hence, this characterized cascade provides the mechanistic basis for interpreting current observations that sesamin modulates MAPK phosphorylation, downregulates MMP expression, and preserves collagen under UVA exposure (Kuo et al., 2020; Prasanth et al., 2020).

By demonstrating that sesamin treatment reduces ROS generation as assessed by DCFH‐DA assay and concomitantly reduces the phosphorylation of MAPKs (ERK, JNK and p38), it was shown that sesamin intervened early in this cascade. The downstream reduction of MMP-1 and preservation of collagen type I or prevention of its degradation further suggest that the upstream inhibition of ROS/MAPK has meaningful ECM outcomes.

Previous studies have reported the protective effects of various natural compounds in UV-induced skin damage models. For example, glycoproteins isolated from sesame seeds were shown to inhibit UV-induced MMP-1 expression, suppress MAPK/AKT activation, and reduce wrinkle formation in hairless mice (Baik et al., 2024). Similarly, carnosine was reported to modulate Nrf2-mediated oxidative stress responses and protect the extracellular matrix in UVA-exposed three-dimensional fibroblast spheroids (Aiello et al., 2022). Collectively, these reports highlight the photoprotective capacity of natural compounds, although direct efficacy comparisons with sesamin are beyond the scope of the present study. A distinguishing aspect of the present study is the direct investigation of sesamin under UVA exposure in human dermal fibroblasts, which reflects the predominant form of solar ultraviolet radiation reaching the dermis and therefore enhances the translational relevance of the current results.

On the other hand, the discovery that sesamin can be found in A. littoricola and it exhibits anti-photoaging potential provides important insights into both undervalued crop utilization and skin health applications. These findings underscore the potential of A. littoricola as a bioactive-rich species suitable for development into cosmeceutical resources. From a dermatological standpoint, sesamin or sesamin-enriched extracts may serve as promising candidates for topical or nutraceutical interventions aimed at protecting the skin against photoaging.

While the present work has aforementioned strengths, it was limited to an in vitro fibroblast model under controlled UVA exposure, which does not fully capture the complexity of human skin or chronic UV conditions. Although the present findings provide clear mechanistic evidence for the anti-photoaging effects of sesamin in human dermal fibroblasts, further validation using three-dimensional skin-equivalent models and in vivo systems will be required to confirm its translational potential. Further mechanistic analyses and donor-diverse fibroblast models would clarify pathway involvement and biological variability, while formulation and delivery studies will be essential to ensure stability, skin penetration, and safety for practical applications.

In conclusion, this study showed that sesamin from A. littoricola attenuated UVA-induced ROS generation, MAPK activation (ERK, JNK, p38), MMP-1 overexpression and potentially preserves dermal ECM integrity via collagen maintenance. This builds on prior evidence of sesamin’s anti-photoaging effect under UVB and adds a UVA/fibroblast dimension, which increases relevance for dermal photoaging. In addition, results support A. littoricola as a functional medicinal crop species with potential for cosmeceutical development. Future studies should include in vivo validation, chronic exposure models, formulation development and mechanistic research. Nevertheless, it was suggested that sesamin’s multi-target mechanism on ROS scavenging, MAPK inhibition and MMP reduction offers a favorable profile and merits further development.

Acknowledgments

This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (No. RS-2023-00212560), and by the Korea Institute of Marine Science & Technology Promotion (KIMST), funded by the Ministry of Oceans and Fisheries, Korea (20220259). NMR spectral data were kindly provided by Dr. Eun-Hee Kim (Korea Basic Science Institute, Daejeon, Korea).

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