Department of Dermatology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Department of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China.
Medicine (Baltimore). 2021 Jan 22;100(3):e23986. doi: 10.1097/MD.0000000000023986.
Rosacea is a facial chronic inflammatory skin disease with immune and vascular system dysfunction. Paeoniflorin (PF) is a traditional Chinese medicine with anti-inflammatory properties. However, its effects on rosacea remain unknown. Here, we investigated the mechanisms through which PF inhibits the macrophage-related rosacea-like inflammatory response. Immunohistochemical methods were used to detect differences in the inflammatory response and degree of macrophage infiltration in granulomatous rosacea lesions and their peripheral areas. Cell Counting Kit-8 was used to determine the cytotoxicity of PF towards RAW 264.7 cells. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to measure the influence of PF on mRNA and protein expression levels of suppressor of cytokine signaling 3 (SOCS3), apoptosis signal-regulating kinase 1 (ASK1)-p38, Toll-like receptor 2, and cathelicidin antimicrobial peptide ( or LL37) in the lipopolysaccharide (LPS)-induced macrophage-related rosacea-like inflammatory response of RAW 264.7 cells. Inflammatory cell infiltration was more pronounced in granulomatous rosacea lesions than in peripheral areas. LL37 expression increased significantly, and the infiltration of a large number of CD68+ macrophages was observed in the lesions. PF promoted SOCS3 expression in RAW 264.7 cells and inhibited the LPS-induced increase in toll-like receptor 2 and LL37 expression through the ASK1-p38 cascade, thereby alleviating the macrophage-related rosacea-like inflammatory response. These changes could be abrogated by SOCS3 siRNA in vitro.In conclusion, the pathogenesis of rosacea involves abnormal macrophage infiltration within the lesions. PF inhibits the macrophage-related rosacea-like inflammatory response through the SOCS3-ASK1-p38 pathway, demonstrating its potential application as a novel drug for rosacea therapy.
酒渣鼻是一种慢性炎症性面部皮肤疾病,具有免疫和血管系统功能障碍。芍药苷(PF)是一种具有抗炎作用的中药。然而,其在酒渣鼻中的作用尚不清楚。在这里,我们研究了 PF 抑制与巨噬细胞相关的酒渣鼻样炎症反应的机制。免疫组织化学方法用于检测肉芽肿性酒渣鼻病变及其周围区域炎症反应和巨噬细胞浸润程度的差异。细胞计数试剂盒-8 用于确定 PF 对 RAW 264.7 细胞的细胞毒性。逆转录定量聚合酶链反应和蛋白质印迹用于测量 PF 对 LPS 诱导的 RAW 264.7 细胞与巨噬细胞相关的酒渣鼻样炎症反应中抑制细胞因子信号转导 3(SOCS3)、凋亡信号调节激酶 1(ASK1)-p38、Toll 样受体 2 和抗菌肽 cathelicidin(或 LL37)的 mRNA 和蛋白表达水平的影响。与外周区域相比,肉芽肿性酒渣鼻病变中的炎症细胞浸润更为明显。LL37 表达显著增加,病变中观察到大量 CD68+巨噬细胞浸润。PF 促进 RAW 264.7 细胞中 SOCS3 的表达,并通过 ASK1-p38 级联抑制 LPS 诱导的 TLR2 和 LL37 表达的增加,从而缓解与巨噬细胞相关的酒渣鼻样炎症反应。这些变化可以通过 SOCS3 siRNA 在体外被阻断。总之,酒渣鼻的发病机制涉及病变内异常的巨噬细胞浸润。PF 通过 SOCS3-ASK1-p38 通路抑制与巨噬细胞相关的酒渣鼻样炎症反应,表明其作为酒渣鼻治疗的新型药物具有潜在应用价值。