Effects of Triacetin on AMPK Activation and Immune Responses in Allergic Contact Dermatitis
Background/Objectives: Allergic contact dermatitis (ACD), an inflammatory skin condition, is commonly treated with topical corticosteroids; however, long-term use of these drugs is associated with various risks, such as skin atrophy and steroid resistance. Triacetin (TA), a triglyceride metabolized...
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MDPI AG
2024-12-01
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| Series: | Allergies |
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| Online Access: | https://www.mdpi.com/2313-5786/4/4/17 |
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| author | Yukihiro Yoshimura Momoka Takahashi |
| author_facet | Yukihiro Yoshimura Momoka Takahashi |
| author_sort | Yukihiro Yoshimura |
| collection | DOAJ |
| description | Background/Objectives: Allergic contact dermatitis (ACD), an inflammatory skin condition, is commonly treated with topical corticosteroids; however, long-term use of these drugs is associated with various risks, such as skin atrophy and steroid resistance. Triacetin (TA), a triglyceride metabolized to acetate, exerts anti-inflammatory affects by activating AMP-activated protein kinase (AMPK) and suppressing mast cell degranulation. Here, we aimed to assess the immediate and long-term effects of TA on ACD suppression, focusing on AMPK activation, using a 2,4-dinitrofluorobenzene-induced rodent model. Methods: Various concentrations of TA were topically applied to rats with 2,4-dinitrofluorobenzene-induced dermatitis. Ear thickness was measured, and histological analysis was performed to assess the inflammation, mast cell infiltration, and degranulation in the established models. AMPK activation was analyzed via Western blotting, and TA degradation was assessed via gas chromatography-mass spectrometry. Dorsomorphin (an AMPK inhibitor) was used to evaluate the effects of AMPK on ACD. Results: TA significantly inhibited inflammation and mast cell degranulation in a dose-dependent manner, with 0.25 mmol/L showing the most potent effects. It also activated AMPK activation. Notably, AMPK inhibition reversed the effects of TA. Conclusions: Overall, TA exerted immediate and long-term anti-inflammatory effects via AMPK activation and inhibition of mast cell degranulation, showing potential as a non-steroidal therapeutic for ACD. |
| format | Article |
| id | doaj-art-fdf3f37b64fa46c4bbc1c010b6e214d4 |
| institution | Kabale University |
| issn | 2313-5786 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Allergies |
| spelling | doaj-art-fdf3f37b64fa46c4bbc1c010b6e214d42024-12-27T14:05:22ZengMDPI AGAllergies2313-57862024-12-014425426710.3390/allergies4040017Effects of Triacetin on AMPK Activation and Immune Responses in Allergic Contact DermatitisYukihiro Yoshimura0Momoka Takahashi1Department of Nutrition, Kobe Gakuin University, 518 Arise, Ikawadani-cho, Nishi-ku, Kobe City 651-2180, JapanDepartment of Nutrition, Kobe Gakuin University, 518 Arise, Ikawadani-cho, Nishi-ku, Kobe City 651-2180, JapanBackground/Objectives: Allergic contact dermatitis (ACD), an inflammatory skin condition, is commonly treated with topical corticosteroids; however, long-term use of these drugs is associated with various risks, such as skin atrophy and steroid resistance. Triacetin (TA), a triglyceride metabolized to acetate, exerts anti-inflammatory affects by activating AMP-activated protein kinase (AMPK) and suppressing mast cell degranulation. Here, we aimed to assess the immediate and long-term effects of TA on ACD suppression, focusing on AMPK activation, using a 2,4-dinitrofluorobenzene-induced rodent model. Methods: Various concentrations of TA were topically applied to rats with 2,4-dinitrofluorobenzene-induced dermatitis. Ear thickness was measured, and histological analysis was performed to assess the inflammation, mast cell infiltration, and degranulation in the established models. AMPK activation was analyzed via Western blotting, and TA degradation was assessed via gas chromatography-mass spectrometry. Dorsomorphin (an AMPK inhibitor) was used to evaluate the effects of AMPK on ACD. Results: TA significantly inhibited inflammation and mast cell degranulation in a dose-dependent manner, with 0.25 mmol/L showing the most potent effects. It also activated AMPK activation. Notably, AMPK inhibition reversed the effects of TA. Conclusions: Overall, TA exerted immediate and long-term anti-inflammatory effects via AMPK activation and inhibition of mast cell degranulation, showing potential as a non-steroidal therapeutic for ACD.https://www.mdpi.com/2313-5786/4/4/17allergic contact dermatitistriacetinacetateAMPK |
| spellingShingle | Yukihiro Yoshimura Momoka Takahashi Effects of Triacetin on AMPK Activation and Immune Responses in Allergic Contact Dermatitis Allergies allergic contact dermatitis triacetin acetate AMPK |
| title | Effects of Triacetin on AMPK Activation and Immune Responses in Allergic Contact Dermatitis |
| title_full | Effects of Triacetin on AMPK Activation and Immune Responses in Allergic Contact Dermatitis |
| title_fullStr | Effects of Triacetin on AMPK Activation and Immune Responses in Allergic Contact Dermatitis |
| title_full_unstemmed | Effects of Triacetin on AMPK Activation and Immune Responses in Allergic Contact Dermatitis |
| title_short | Effects of Triacetin on AMPK Activation and Immune Responses in Allergic Contact Dermatitis |
| title_sort | effects of triacetin on ampk activation and immune responses in allergic contact dermatitis |
| topic | allergic contact dermatitis triacetin acetate AMPK |
| url | https://www.mdpi.com/2313-5786/4/4/17 |
| work_keys_str_mv | AT yukihiroyoshimura effectsoftriacetinonampkactivationandimmuneresponsesinallergiccontactdermatitis AT momokatakahashi effectsoftriacetinonampkactivationandimmuneresponsesinallergiccontactdermatitis |