Zheng Nana, Zhou Meng, He Yanyan, Xu Haoxiang, Chen Xu, Duan Zhimin, Yang Lu, Zeng Rong, Liu Yuzhen, Li Min
Institute of Dermatology, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Hospital for Skin Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, China; Graduate School of Peking Union Medical College, China.
Institute of Dermatology, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Hospital for Skin Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, China.
Photodiagnosis Photodyn Ther. 2022 Dec;40:103204. doi: 10.1016/j.pdpdt.2022.103204. Epub 2022 Nov 17.
Curcumin has been employed as a photosensitizer agent during photodynamic therapy (PDT). Cutibacterium acnes (C. acnes) can cause an inflammatory response in human keratinocytes; however, no research has been conducted to determine whether curcumin and its photodynamic properties can prevent this inflammatory reaction.
We hypothesized that curcumin may control the C. acnes biofilm-induced inflammatory response in keratinocytes, either alone or in combination with blue light photodynamic therapy.
Following C. acnes biofilm stimulation, human primary keratinocytes were treated with 20 μM curcumin solution alone or 5 μM curcumin with combined blue light irradiation. The amount of secreted protein was measured using an ELISA kit. The expression levels of Toll-like receptor 2 (TLR2) and its downstream proteins were determined using western blot.
Treatment with 20 μM curcumin, but not 5 μM curcumin, reduced the inflammatory response to C. acnes biofilms in keratinocytes by blocking the TLR2/MAPK/NF-κB pathway. Interestingly, 5 μM curcumin combined with blue light also reduced the C. acnes biofilm-induced inflammation indicated above by blocking the TLR2/MAPK/NF-κB pathway.
Curcumin alone, in sufficient concentrations, or low-concentration curcumin with blue light had anti-inflammatory activity on keratinocytes stimulated by C. acnes biofilms through inhibition of MAPK and NF-κB signaling pathways by downregulating TLR2 expression.
姜黄素已被用作光动力疗法(PDT)中的光敏剂。痤疮丙酸杆菌(C. acnes)可在人角质形成细胞中引发炎症反应;然而,尚未开展研究来确定姜黄素及其光动力特性是否能预防这种炎症反应。
我们假设姜黄素可能单独或与蓝光光动力疗法联合控制痤疮丙酸杆菌生物膜诱导的角质形成细胞炎症反应。
在痤疮丙酸杆菌生物膜刺激后,人原代角质形成细胞分别用20μM姜黄素溶液单独处理或5μM姜黄素联合蓝光照射处理。使用酶联免疫吸附测定试剂盒测量分泌蛋白的量。使用蛋白质印迹法测定Toll样受体2(TLR2)及其下游蛋白的表达水平。
20μM姜黄素处理而非5μM姜黄素处理通过阻断TLR2/MAPK/NF-κB途径降低了角质形成细胞对痤疮丙酸杆菌生物膜的炎症反应。有趣的是,5μM姜黄素与蓝光联合也通过阻断TLR2/MAPK/NF-κB途径降低了上述痤疮丙酸杆菌生物膜诱导的炎症。
单独使用足够浓度的姜黄素或低浓度姜黄素与蓝光对痤疮丙酸杆菌生物膜刺激的角质形成细胞具有抗炎活性,其通过下调TLR2表达抑制MAPK和NF-κB信号通路。