Department of Chinese Medicine Property Team, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
Guangdong Province Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, Guangzhou, Guangdong 510115, P.R. China.
Mol Med Rep. 2018 Mar;17(3):3789-3796. doi: 10.3892/mmr.2017.8343. Epub 2017 Dec 22.
Astilbin has anti-inflammatory and immunoregulatory effects, and is frequently used in prescriptions treating psoriasis; however, the mechanism remains to be fully elucidated. In the present study, the effect of an astilbin microemulsion on a psoriasis‑like model in guinea pigs was examined, and the underlying mechanism was investigated. The levels of interkeukin (IL)‑6, IL‑17A and IL‑22 were determined using fluorescent reverse transcription‑quantitative polymerase chain reaction analysis and enzyme‑linked immunosorbent assays. The phosphorylation of p38 and extracellular signal‑regulated kinase (ERK)1/2 was detected using western blot analysis. Compared with the untreated control, astilbin significantly ameliorated the lesions induced by propranolol hydrochloride. The effect of astilbin on cytokine levels were cytokine‑ and drug‑concentration‑dependent. At a concentration of 2.22 µM, astilbin decreased the mRNA expression levels of IL‑6, IL‑17A and IL‑22 in lipopolysaccharide (LPS)‑induced HaCaT cells by 89, 69.1 and 69.3%, respectively. However, 2.22 µM astilbin had no effect on the protein expression of IL‑17A, and decreased the protein expression levels of IL‑6 and IL‑22 by 79.2 and 49.5%, respectively (P<0.05). At a concentration of 11.10 µM, astilbin decreased the mRNA expression of IL‑6, which was significantly induced by LPS, and significantly (P<0.05) decreased the protein expression levels of IL‑6 and IL‑22. Additionally, astilbin inhibited the LPS‑induced activation of phosphorylated p38. These results suggested that astilbin has the potential to be developed into a topical drug for the treatment of psoriasis via the inhibition of inflammatory cytokines.
梓醇具有抗炎和免疫调节作用，常用于治疗银屑病的方剂中；然而，其作用机制尚不完全清楚。本研究考察了梓醇微乳对豚鼠银屑病样模型的作用，并探讨了其作用机制。采用荧光逆转录定量聚合酶链反应分析和酶联免疫吸附试验测定白细胞介素（IL）-6、IL-17A 和 IL-22 的水平。采用 Western blot 分析检测 p38 和细胞外信号调节激酶（ERK）1/2 的磷酸化水平。与未处理的对照组相比，梓醇可显著改善盐酸普萘洛尔诱导的病变。梓醇对细胞因子水平的影响与细胞因子和药物浓度有关。在 2.22µM 浓度下，梓醇分别使脂多糖（LPS）诱导的 HaCaT 细胞中 IL-6、IL-17A 和 IL-22 的 mRNA 表达水平降低 89%、69.1%和 69.3%。然而，2.22µM 梓醇对 IL-17A 的蛋白表达没有影响，使 IL-6 和 IL-22 的蛋白表达水平分别降低 79.2%和 49.5%（P<0.05）。在 11.10µM 浓度下，梓醇降低了 LPS 显著诱导的 IL-6 的 mRNA 表达，并显著（P<0.05）降低了 IL-6 和 IL-22 的蛋白表达水平。此外，梓醇抑制了 LPS 诱导的磷酸化 p38 的激活。这些结果表明，梓醇通过抑制炎症细胞因子，有可能被开发为治疗银屑病的局部药物。
