College of Pharmacy and Wonkwang-Oriental Medicines Research Institute, Wonkwang University, Iksan, Jeonbuk, Korea
Eur Rev Med Pharmacol Sci. 2012 Sep;16(9):1184-91.
Sinomenine is an alkaloid compound and a prominent anti-inflammatory agent found in the root of the climbing plant Sinomenium acutum. However, its effects on the mechanism of human mast cell line (HMC)-1-mediated inflammation remained unknown.
To provide insight into the biological effects of sinomenine, we examined its influence on the pro-inflammatory cytokine production in HMC-1 cells stimulated by phorbol 12-myristate-13-acetate (PMA) plus A23187 by evaluating the stimulated cells in the presence or absence of sinomenine. In the present study, the pro-inflammatory cytokine production was measured using ELISA, Reverse Transcription-polymerase chain reaction (RT-PCR) and nuclear factor (NF)-kappaB, mitogen-activated protein kinases (MAPKs) pathway activation, as determined by Western blot analysis. Also, cyclooxygenase (COX)-2 expression was measured through Western blot and RT-PCR analysis.
Sinomenine inhibited the pro-inflammatory cytokine production induced by PMA plus A23187 in a dose-dependent manner. Furthermore, sinomenine inhibited the phosphorylations of extracellular signal-regulated kinase (ERK) and p38 MAPKs as well as the translocation of NF-kappaB p65 through reduced IkappaBalpha degradation. In addition, sinomenine suppressed COX-2 protein and mRNA expression dose-dependently.
Taken together, the results of this study indicate that the anti-inflammatory effects of sinomenine may occur via the inhibition of pro-inflammatory cytokine and COX-2 production through the inhibition of MAPKs and NF-kappaB pathway activation by PMA plus A23187 stimulation in HMC-1 cells.
青藤碱是一种生物碱化合物，是从青风藤中提取的一种主要的抗炎物质。然而，其对人肥大细胞株（HMC-1）介导的炎症的作用机制尚不清楚。
为了深入了解青藤碱的生物学作用，我们研究了青藤碱对佛波醇 12-肉豆蔻酸 13-乙酸酯（PMA）加 A23187 刺激的 HMC-1 细胞中促炎细胞因子产生的影响，在有无青藤碱的情况下评估刺激的细胞。在本研究中，通过酶联免疫吸附试验（ELISA）、逆转录-聚合酶链反应（RT-PCR）和核因子（NF）-κB、丝裂原激活蛋白激酶（MAPKs）通路激活的 Western blot 分析来测量促炎细胞因子的产生。此外，通过 Western blot 和 RT-PCR 分析来测量环氧化酶（COX）-2 的表达。
青藤碱呈剂量依赖性抑制 PMA 加 A23187 诱导的促炎细胞因子产生。此外，青藤碱通过减少 IkappaBalpha 的降解来抑制细胞外信号调节激酶（ERK）和 p38 MAPKs 的磷酸化以及 NF-κB p65 的转位。此外，青藤碱呈剂量依赖性抑制 COX-2 蛋白和 mRNA 的表达。
综上所述，本研究结果表明，青藤碱的抗炎作用可能是通过抑制 PMA 加 A23187 刺激的 HMC-1 细胞中促炎细胞因子和 COX-2 的产生，从而抑制 MAPKs 和 NF-κB 通路的激活。
