Department of Medical Cosmetology, Dermatology Hospital of Southern Medical University, Guangzhou, China.
Department of Medical Cosmetology, Dermatology Hospital of Southern Medical University, Guangzhou, China,
Skin Pharmacol Physiol. 2023;36(2):98-106. doi: 10.1159/000529551. Epub 2023 Feb 6.
The role of bone marrow mesenchymal stem cells-derived exosomes (BMSCs-exo) in skin photoaging was explored in human dermal fibroblasts (HDFs). The underlying mechanism was further explored.
HDFs were exposed to UVB irradiation to establish the cell photodamage models. The cell viability and levels of oxidative stress-related factors were tested. ELISA was done to detect TNF-α, IL-6, and IL-1β concentrations. Western blot was applied for protein examination.
UVB treatment led to the inhibition of cell viability. But after BMSCs-exo addition, the inhibitory effect was returned in a dose manner. UVB exposure contributed to the increase of reactive oxygen species and LDH and the downregulation of superoxide dismutase. In addition, excessive secretion of TNF-α, IL-6, and IL-1β was also detected in cells exposed to UVB. However, BMSCs-exo addition eliminated the effects of UVB on oxidative stress and inflammation in HDFs. BMSCs-exo inhibited matrix metalloproteinases MMP-1 and MMP-3 expression but promoted collagen I expression. UVB radiation activated the MAPK/AP-1 signaling, manifested as the increase of p-p38, c-Jun, and c-Fos protein levels, which were reversed by BMSCs-exo. As a p38 agonist, anisomycin counteracted the effect of BMSCs-exo on HDF's viability, oxidative stress, and inflammation.
BMSCs-exo protected HDFs against UVB-induced inhibition of cell viability and the activation of cell oxidative stress and inflammation, which might be related to the inhibition of the MAPK/AP-1 signaling pathway.
本研究旨在探讨骨髓间充质干细胞来源的外泌体（BMSCs-exo）在人真皮成纤维细胞（HDFs）皮肤光老化中的作用，并进一步探讨其作用机制。
用 UVB 辐射处理 HDFs 建立细胞光损伤模型，检测细胞活力和氧化应激相关因子水平，用 ELISA 法检测 TNF-α、IL-6 和 IL-1β 浓度，用 Western blot 法检测蛋白表达。
UVB 处理导致细胞活力抑制，但 BMSCs-exo 处理呈剂量依赖性恢复抑制作用。UVB 暴露导致活性氧和 LDH 增加，超氧化物歧化酶下调，此外，还检测到 UVB 暴露的细胞中 TNF-α、IL-6 和 IL-1β 过度分泌。然而，BMSCs-exo 处理消除了 UVB 对 HDFs 氧化应激和炎症的影响。BMSCs-exo 抑制基质金属蛋白酶 MMP-1 和 MMP-3 的表达，但促进胶原 I 的表达。UVB 辐射激活 MAPK/AP-1 信号通路，表现为 p-p38、c-Jun 和 c-Fos 蛋白水平增加，BMSCs-exo 处理可逆转这一变化。作为 p38 激动剂，anisomycin 拮抗 BMSCs-exo 对 HDF 活力、氧化应激和炎症的作用。
BMSCs-exo 可保护 HDFs 免受 UVB 诱导的细胞活力抑制、细胞氧化应激和炎症激活，这可能与 MAPK/AP-1 信号通路的抑制有关。
