Herbal Medicine Division, Korea Institute of Oriental Medicine.
Department of Korean Life Science and Technology, University of Science and Technology.
Biol Pharm Bull. 2019 Sep 1;42(9):1524-1531. doi: 10.1248/bpb.b19-00222. Epub 2019 Jul 2.
UVB radiation changes several photoaging pathway in the body, thereby prompting skin injury. Besides, chronic UVB radiation leads to photoaging, sustained immunosuppression, and photocarcinogenesis. We investigated the protective effect of Timosaponin AIII (TA-III), a naturally occurring steroidal saponin separated from Anemarrhena asphodeloides, against UVB-induced invasive properties of human epidermal keratinocytes (HEKs) and human dermal fibroblasts (HDF). No cytotoxicity was observed up to 50 nM concentration of TA-III. Similarly, TA-III inhibited UVB-induced cyclooxygenase-2 (COX-2), matrix metalloproteinase-9 (MMP-9) transcription level and protein expression in a dose-dependent manner at non-cytotoxic dose. Further, TA-III decreased UVB-induced invasion in primary skin cells. Additionally, TA-III suppressed UVB-stimulates mitogen-activated protein kinase (MAPK) signaling, activator protein-1 (AP-1) and nuclear factor kappa B (NF-κB) activation, thereby preventing the overexpression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and COX-2 in human epidermal keratinocytes cells. Furthermore, TA-III prevented UVB-mediated formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dG) and activation of DNA repair enzymes and, cell cycle arrest genes like as proliferating cell nuclear antigen (PCNA), structural maintenance of chromosomes protein 1 (SMC1). This results support that understanding into the molecular action of TA-III, which can be useful for developing photoprotective agents.
中波紫外线（UVB）辐射会改变体内的多种光老化途径，从而引发皮肤损伤。此外，慢性中波紫外线辐射会导致光老化、持续的免疫抑制和光致癌发生。我们研究了从知母中分离得到的天然甾体皂苷提木皂苷 AIII（TA-III）对人表皮角质形成细胞（HEK）和人真皮成纤维细胞（HDF）的 UVB 诱导侵袭特性的保护作用。高达 50 nM 的 TA-III 浓度下未观察到细胞毒性。同样，TA-III 在非细胞毒性剂量下以剂量依赖性方式抑制 UVB 诱导的环氧合酶-2（COX-2）、基质金属蛋白酶-9（MMP-9）转录水平和蛋白表达。此外，TA-III 降低了原发性皮肤细胞的 UVB 诱导侵袭。此外，TA-III 抑制了 UVB 刺激的丝裂原活化蛋白激酶（MAPK）信号、激活蛋白-1（AP-1）和核因子 kappa B（NF-κB）的激活，从而防止肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和 COX-2 在人表皮角质形成细胞中的过度表达。此外，TA-III 可防止 UVB 介导的 8-氧代-7,8-二氢-2'-脱氧鸟苷（8-oxo-dG）形成和 DNA 修复酶以及细胞周期停滞基因如增殖细胞核抗原（PCNA）、染色体结构维持蛋白 1（SMC1）的激活。这些结果支持了对 TA-III 分子作用的理解，这对于开发光保护剂可能是有用的。
