Wang H, Qi J, Li L, Wu T, Wang Y, Wang X, Ning Q
Department of Infectious Disease, Institute of Infectious Disease, Tongji hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China.
Department of Infectious Disease, Institute of Infectious Disease, Tongji hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
Int J Immunopathol Pharmacol. 2015 Sep;28(3):308-17. doi: 10.1177/0394632015589519. Epub 2015 Jul 8.
This study investigated anti-inflammatory effects and possible mechanisms of Chikusetsusaponin IVa (Chi IVa), one of the main bioactive components in saponins from Panacis japonica (SPJ), which is used in traditional Tujia and Hmong Chinese medicine. To this end, changes in the inflammatory profiles of lipopolysacchride (LPS)-stimulated phrobol 12-myristate 13-acetate(PMA)-differented THP-1 macrophages were evaluated following Chi IVa treatment. The results showed that Chi IVa markedly decreased the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) at both the mRNA and protein level, which proved to be dose-dependent. Further studies revealed that Chi IVa strongly suppressed NF-κB activation and downregulated the phosphorylation of ERK, p38, and JNK. Our present study demonstrates that Chi IVa suppresses the production of iNOS, COX-2, IL-1β, IL-6, and TNF-α in LPS-stimulated THP-1 cells likely by inhibiting NF-κB activation and ERK, JNK, and p38 signal pathway phosphorylation.
本研究调查了竹节人参皂苷IVa(Chi IVa)的抗炎作用及其可能机制。Chi IVa是竹节人参皂苷(SPJ)中的主要生物活性成分之一,在土家族和苗族传统中药中使用。为此,在Chi IVa处理后,评估了脂多糖(LPS)刺激的佛波醇12-肉豆蔻酸酯13-乙酸酯(PMA)分化的THP-1巨噬细胞炎症谱的变化。结果表明,Chi IVa在mRNA和蛋白质水平上均显著降低了诱导型一氧化氮合酶(iNOS)、环氧化酶-2(COX-2)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的表达,且呈剂量依赖性。进一步研究表明,Chi IVa强烈抑制NF-κB激活,并下调ERK、p38和JNK的磷酸化。我们目前的研究表明,Chi IVa可能通过抑制NF-κB激活以及ERK、JNK和p38信号通路磷酸化来抑制LPS刺激的THP-1细胞中iNOS、COX-2、IL-1β、IL-6和TNF-α的产生。