当前位置: X-MOL 学术Mediat. Inflamm. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Saponin from Periploca forrestii Schltr Mitigates Oxazolone-Induced Atopic Dermatitis via Modulating Macrophage Activation
Mediators of Inflammation ( IF 4.6 ) Pub Date : 2020-10-15 , DOI: 10.1155/2020/4346367
Luting Zeng 1 , Yingqin Liu 2 , Congcong Xing 1 , Yijie Huang 1 , Xin Sun 3 , Guangchen Sun 1
Affiliation  

Atopic dermatitis (AD) is a relapsing, acute, and chronic skin disease featured by intractable itching, eczematous skin. Conventional therapies based on immunosuppression such as corticosteroids are associated with multiple adverse reactions. Periploca forrestii Schltr saponin (PFS) was shown to potently inhibit murine arthritis by protecting bone and cartilage injury and suppressing NF-κB activation. However, its therapeutic effect on oxazolone-induced atopic dermatitis (AD) and the underlying mechanisms on macrophage are still unclear. The AD-like dermatitis was induced by repeated oxazolone challenge to the skin of BALB/c mice in vivo. Blood and ears were biochemically or histologically processed. RT-PCR, western blotting, and ELISA were conducted to evaluate the expression of macrophage factors. Mouse bone marrow-derived macrophages (BMDMs) stimulated with lipopolysaccharide (LPS) were used as a model in vitro. PFS treatment inhibited AD-like dermatitis development. PFS downregulated epidermis thickness and cell infiltration, with histological analysis of the skin lesion. PFS alleviated plasma immunoglobulin (Ig) E, IgG2a, and IgG1 levels. PFS downregulated the expression of M1 macrophage factors, tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, monocyte chemotactic protein-1 (MCP-1), and nitric oxide synthase2 (NOS2), and M2 macrophage factors, IL-4, arginase1 (Arg1) and CD163 in AD-like skin, which were confirmed by western blot and ELISA analysis. In addition, PFS inhibited LPS-induced macrophage polarization via the inhibition of the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and nuclear translocation of NF-κB p65. These results suggest that PFS exerted an antidermatitis effect against oxazolone by modulating macrophage activation. PFS administration might be useful in the treatment of AD and inflammatory skin diseases.

中文翻译:

来自 Periploca forrestii Schltr 的皂苷通过调节巨噬细胞活化减轻恶唑酮诱导的特应性皮炎

特应性皮炎 (AD) 是一种复发性、急性和慢性皮肤病,其特征是顽固性瘙痒、皮肤湿疹。基于免疫抑制的常规疗法如皮质类固醇与多种不良反应有关。Periploca forrestii Schltr 皂苷 (PFS) 被证明通过保护骨和软骨损伤并抑制 NF- κ来有效抑制鼠关节炎B 激活。然而,其对恶唑酮诱导的特应性皮炎(AD)的治疗作用和巨噬细胞的潜在机制仍不清楚。AD 样皮炎是由体内 BALB/c 小鼠皮肤反复恶唑酮攻击诱发的。血液和耳朵经过生物化学或组织学处理。进行RT-PCR、蛋白质印迹和ELISA以评估巨噬细胞因子的表达。用脂多糖 (LPS) 刺激的小鼠骨髓源性巨噬细胞 (BMDM) 作为体外模型。PFS 治疗抑制了 AD 样皮炎的发展。PFS 下调表皮厚度和细胞浸润,对皮肤病变进行组织学分析。PFS 减轻了血浆免疫球蛋白 (Ig) E、IgG2a 和 IgG1 水平。PFS 下调 M1 巨噬细胞因子、肿瘤坏死因子- (TNF-) 的表达AD样皮肤中的α、白细胞介素-(IL-)6、单核细胞趋化蛋白-1(MCP-1)和一氧化氮合酶2(NOS2)和M2巨噬细胞因子、IL-4、精氨酸酶1(Arg1)和CD163,经蛋白质印迹和ELISA分析证实。此外,PFS抑制经由信号转导和转录因子3(STAT3)和NF-的核易位的活化剂的磷酸化的抑制LPS诱导的巨噬细胞极化κ乙P65。这些结果表明 PFS 通过调节巨噬细胞活化对恶唑酮发挥抗皮炎作用。PFS 给药可能有助于治疗 AD 和炎症性皮肤病。
更新日期:2020-10-16
down
wechat
bug