Emodin and aloe-emodin are two anthraquinones having positive effects in wound healing. However, their mechanism of action of wound healing is not fully understood. The MAP kinase family, which plays an active role in wound healing, is a well-characterized large family of serine/threonine kinases and regulates processes such as proliferation, oncogenesis, differentiation, and inflammation in the cell. The aim of this study is to comparatively elucidate the mechanisms of action of emodin and aloe-emodin, which are potential agents in wound healing. The mechanism of the effects of emodin and aloe-emodin on cell viability and cell migration was examined using the human skin fibroblast (CCD-1079Sk) cell line. The gene expression levels of the MAP kinases (JNK, P38, ERK) in the skin fibroblast cells along with a molecular docking study analyzing their interaction potential were evaluated. Furthermore, the molecules’ effects on the lifespan of Caenorhabditis elegans were studied. Emodin and aloe-emodin inhibited the ATP content of the cells in a concentration dependent manner and accelerated cell migration at the lower concentrations while inhibiting cell migration in the higher concentration treatment groups. The expressions of JNK and P38 were upregulated at the low concentrations and downregulated at the higher concentrations. The molecular docking studies of the molecules gave high docking scores indicating their interaction potential with JNK and P38. C. elegans lifespan under heat stress was observed longer after 75 µM emodin and was significantly reduced after 150 µM aloe-emodin treatment. Aloe-emodin was found to be more potent on cell viability, cell migration, gene expression levels of the MAP kinases in healthy fibroblastic skin cells, and on the lifespan of C. elegans. This study reveals the functional effects and the biological factors that interact in the wound healing process of emodin and aloe-emodin, and give a possible treatment alternative to shorten the duration of wound care.

中文翻译：

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大黄素和芦荟大黄素是通过 MAP 激酶途径调节皮肤细胞迁移并影响秀丽隐杆线虫耐热性的两种潜在分子

大黄素和芦荟大黄素是两种对伤口愈合具有积极作用的蒽醌类化合物。然而，它们促进伤口愈合的作用机制尚不完全清楚。MAP 激酶家族在伤口愈合中发挥积极作用，是一个特征明确的丝氨酸/苏氨酸激酶大家族，调节细胞增殖、肿瘤发生、分化和炎症等过程。本研究的目的是比较阐明大黄素和芦荟大黄素的作用机制，它们是伤口愈合的潜在药物。使用人皮肤成纤维细胞 (CCD-1079Sk) 细胞系检查大黄素和芦荟大黄素对细胞活力和细胞迁移的影响机制。评估了皮肤成纤维细胞中 MAP 激酶（JNK、P38、ERK）的基因表达水平以及分析它们相互作用潜力的分子对接研究。此外，还研究了这些分子对秀丽隐杆线虫寿命的影响。大黄素和芦荟大黄素以浓度依赖性方式抑制细胞的ATP含量，并在较低浓度下加速细胞迁移，而在较高浓度处理组中抑制细胞迁移。JNK和P38的表达在低浓度下上调，在高浓度下下调。这些分子的分子对接研究给出了高对接分数，表明它们与 JNK 和 P38 的相互作用潜力。在 75 µM 大黄素处理后，线虫在热应激下的寿命延长，而在 150 µM 芦荟大黄素处理后显着缩短。研究发现，芦荟大黄素对健康成纤维细胞皮肤细胞中的细胞活力、细胞迁移、MAP 激酶基因表达水平以及线虫的寿命更有效。这项研究揭示了大黄素和芦荟大黄素在伤口愈合过程中相互作用的功能效应和生物学因素，并为缩短伤口护理时间提供了可能的治疗替代方案。