ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Experimental Pharmacology and Drug Discovery
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1584233
This article is part of the Research TopicPrevention and Treatment of Skin DiseasesView all 11 articles
Aloin protects against UVB-induced apoptosis by modulating integrated signaling pathways
Provisionally accepted
- 1School of Public Health, Fujian Medical University, Fuzhou, Fujian Province, China
- 2The School of Public Health and Medical Technology, Xiamen Medical College, Xiamen, China
- 3Key Laboratory of Functional and Clinical Translational Medicine, Xiamen, Fujian Province, China
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Aloin, an anthraquinone compound, is naturally abundant in the Aloe. This study comprehensively investigates the photoprotective effects of aloin against UVB-induced damage in HaCaT cells, elucidating its antioxidant capacity and its role in preventing cellular apoptosis. Aloin demonstrated significant antioxidant activity in ABTS and DPPH assays, with a dose-dependent reduction in intracellular ROS levels as evidenced by fluorescence analysis. Western blot analysis revealed that aloin inhibited the phosphorylation of both p38 and JNK, with a more pronounced effect on p38. This was further supported by IC50 values, indicating a higher inhibitory potency of aloin against p38 compared to JNK. Assessments using MTT, Hoechst, Calcein/PI staining, and flow cytometry collectively verified that aloin effectively mitigated UVB-induced apoptosis in cells. Proteomic analysis showed that aloin modulated the expression of proteins involved in critical signaling pathways, including PI3K-Akt, p53, TGF-β and pathways in cancer, promoting cell survival. Aloin upregulated proteins associated with cell cycle regulation and antioxidant responses, such as CCND3, GSTM4, GNA12, SKIL, YWHAZ, and PKN3 while downregulating pro-apoptotic protein FOXO3. These findings highlight aloin's potential as a therapeutic agent for UVB-induced skin damage by effectively modulating cellular stress responses.
Keywords: Aloin, ROS, UVB-induced apoptosis, p38, FOXO3
Received: 27 Feb 2025; Accepted: 23 Jun 2025.
Copyright: © 2025 He, Chen, Wu, Wu, Li, Li and Chen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Yu-Pei Chen, The School of Public Health and Medical Technology, Xiamen Medical College, Xiamen, China
Fangfang Chen, The School of Public Health and Medical Technology, Xiamen Medical College, Xiamen, China
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