New Asperterol from the coral associated fungus Aspergillus terreus, which protects against UVB induced damage through antioxidant, anti-inflammatory, and barrier repair mechanisms.
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| Main Authors: | , , |
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| Format: | Artículo científico |
| Language: | en |
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Journal of photochemistry and photobiology. B, Biology
2025
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| _version_ | 1868266127710224385 |
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| author | Tang, Guangming Zhang, Yi Qian, Zhong-Ji |
| author_facet | Tang, Guangming Zhang, Yi Qian, Zhong-Ji Tang, Guangming Zhang, Yi Qian, Zhong-Ji |
| collection | PubMed - marine biology |
| contents | New Asperterol from the coral associated fungus Aspergillus terreus, which protects against UVB induced damage through antioxidant, anti-inflammatory, and barrier repair mechanisms. Tang, Guangming Zhang, Yi Qian, Zhong-Ji Ultraviolet Rays Humans Anti-Inflammatory Agents Aspergillus Animals Antioxidants Anthozoa Filaggrin Proteins Apoptosis Cell Survival NF-E2-Related Factor 2 Molecular Docking Simulation Reactive Oxygen Species NF-kappa B Keratinocytes Signal Transduction Oxidative Stress Cell Line HaCaT Cells Ultraviolet B (UVB) radiation, a primary cause of skin photoaging, triggers oxidative stress, inflammation, barrier dysfunction, and apoptosis in keratinocytes. New marine-derived benzaldehyde compound B-1 (Asperterrol), isolated from the coral-associated fungus Aspergillus terreus C23-3, has been demonstrated to have multifaceted protective effects against UVB-induced photoaging in HaCaT keratinocytes. This study revealed that B-1 restores cell viability at concentrations ranging from 2.5 to 10 μM and significantly reduces ROS overproduction, particularly at 10 μM, comparable to untreated controls. Mechanistically, B-1 activated the Nrf2/HO-1 antioxidant pathway by promoting Nrf2 nuclear translocation and enhancing superoxide dismutase (SOD-1) expression, as evidenced by molecular docking showing stable hydrogen bonding with nuclear factor (Nrf2) residues (Val606 and Ile559). Concurrently, B-1 suppressed ultraviolet radiation B (UVB)-triggered inflammation via dose-dependent inhibition of inhibitor of NF-kB alpha (IκBα) phosphorylation and NF-κB/MAPK signaling, reducing cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and IL-1β levels. Notably, B-1 upregulated skin barrier proteins Filaggrin and Involucrin, thereby counteracting UVB-induced barrier dysfunction. Furthermore, B-1 further mitigated apoptosis by normalizing the Bcl-2/Bax ratio and suppressing caspase-3 and caspase-9 activation while enhancing early-stage cell migration. These findings underscore the potential of B-1 as a promising multitarget agent against UVB-driven skin damage, bridging marine fungal resources to dermatological innovation. |
| format | Artículo científico |
| id | pubmed_41240726 |
| institution | PubMed |
| language | en |
| publishDate | 2025 |
| publisher | Journal of photochemistry and photobiology. B, Biology |
| record_format | pubmed |
| spellingShingle | New Asperterol from the coral associated fungus Aspergillus terreus, which protects against UVB induced damage through antioxidant, anti-inflammatory, and barrier repair mechanisms. Tang, Guangming Zhang, Yi Qian, Zhong-Ji Ultraviolet Rays Humans Anti-Inflammatory Agents Aspergillus Animals Antioxidants Anthozoa Filaggrin Proteins Apoptosis Cell Survival NF-E2-Related Factor 2 Molecular Docking Simulation Reactive Oxygen Species NF-kappa B Keratinocytes Signal Transduction Oxidative Stress Cell Line HaCaT Cells New Asperterol from the coral associated fungus Aspergillus terreus, which protects against UVB induced damage through antioxidant, anti-inflammatory, and barrier repair mechanisms. Tang, Guangming Zhang, Yi Qian, Zhong-Ji Ultraviolet Rays Humans Anti-Inflammatory Agents Aspergillus Animals Antioxidants Anthozoa Filaggrin Proteins Apoptosis Cell Survival NF-E2-Related Factor 2 Molecular Docking Simulation Reactive Oxygen Species NF-kappa B Keratinocytes Signal Transduction Oxidative Stress Cell Line HaCaT Cells Ultraviolet B (UVB) radiation, a primary cause of skin photoaging, triggers oxidative stress, inflammation, barrier dysfunction, and apoptosis in keratinocytes. New marine-derived benzaldehyde compound B-1 (Asperterrol), isolated from the coral-associated fungus Aspergillus terreus C23-3, has been demonstrated to have multifaceted protective effects against UVB-induced photoaging in HaCaT keratinocytes. This study revealed that B-1 restores cell viability at concentrations ranging from 2.5 to 10 μM and significantly reduces ROS overproduction, particularly at 10 μM, comparable to untreated controls. Mechanistically, B-1 activated the Nrf2/HO-1 antioxidant pathway by promoting Nrf2 nuclear translocation and enhancing superoxide dismutase (SOD-1) expression, as evidenced by molecular docking showing stable hydrogen bonding with nuclear factor (Nrf2) residues (Val606 and Ile559). Concurrently, B-1 suppressed ultraviolet radiation B (UVB)-triggered inflammation via dose-dependent inhibition of inhibitor of NF-kB alpha (IκBα) phosphorylation and NF-κB/MAPK signaling, reducing cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and IL-1β levels. Notably, B-1 upregulated skin barrier proteins Filaggrin and Involucrin, thereby counteracting UVB-induced barrier dysfunction. Furthermore, B-1 further mitigated apoptosis by normalizing the Bcl-2/Bax ratio and suppressing caspase-3 and caspase-9 activation while enhancing early-stage cell migration. These findings underscore the potential of B-1 as a promising multitarget agent against UVB-driven skin damage, bridging marine fungal resources to dermatological innovation. |
| title | New Asperterol from the coral associated fungus Aspergillus terreus, which protects against UVB induced damage through antioxidant, anti-inflammatory, and barrier repair mechanisms. |
| topic | Ultraviolet Rays Humans Anti-Inflammatory Agents Aspergillus Animals Antioxidants Anthozoa Filaggrin Proteins Apoptosis Cell Survival NF-E2-Related Factor 2 Molecular Docking Simulation Reactive Oxygen Species NF-kappa B Keratinocytes Signal Transduction Oxidative Stress Cell Line HaCaT Cells |
| url | https://pubmed.ncbi.nlm.nih.gov/41240726/ |