There are few reports on the biological activities of chaetoglobosin V_b (Cha V_b) (a cytochalasin alkaloid). In this study, we investigated the molecular mechanisms underlying the anti-inflammatory and antioxidant effects of Cha V_b in the RAW264.7 cells stimulated lipopolysaccharide (LPS). LPS stimulation-induced oxidative stress (i.e. increase production of reactive oxygen species (ROS) and decreased expression of antioxidant superoxide dismutase (SOD)) was suppressed after a Cha V_b treatment. Cha V_b could significantly inhibit the upregulated expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) gene and protein induced by LPS whilst attenuating the production of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β. Such antioxidant and anti-inflammatory effects were achieved through the TLR4-mediated MyD88-dependent signaling pathways (via suppressing the phosphorylation of p38, ERK, JNK MAPK and translocation of the NF-κB p65 subunit into nucleus), and the TRIF-dependent signaling pathways (via reducing IFN-β release without inhibiting interferon-regulated factor 3 (IRF3) and IRF7). At 25–100 μM (a concentration range with no cytotoxicity), Cha V_b dose-dependently influenced SOD enzyme activity and phosphorylation of p38, ERK1/2 and JNK, and at 100 μM, likely exerted the greatest inhibition towards LPS-induced oxidative stress and inflammatory response via the MAPK and NF-κB signaling pathway.

关于chaetoglobosin V _b（Cha V _b）（一种细胞松弛素生物碱）的生物学活性的报道很少。在这项研究中，我们调查了ChaV _b在RAW264.7细胞刺激的脂多糖（LPS）中抗炎和抗氧化作用的分子机制。Cha V _b处理后，LPS刺激诱导的氧化应激（即增加活性氧（ROS）的产生和减少抗氧化剂超氧化物歧化酶（SOD）的表达）受到抑制。查V _b能够明显抑制LPS诱导的一氧化氮合酶（iNOS）和环氧合酶-2（COX-2）基因及蛋白的表达上调，同时减弱促炎细胞因子TNF - α，IL-6和IL- 1β的产生。通过TLR4介导的MyD88依赖性信号传导途径（通过抑制p38，ERK，JNK MAPK的磷酸化和NF-κBp65亚基向核内的转运）和TRIF依赖性信号传导可实现此类抗氧化和抗炎作用。途径（通过减少IFN- β释放而不抑制干扰素调节因子3（IRF3）和IRF7）。在25–100μM（浓度范围，无细胞毒性）下，Cha V _b剂量依赖性地影响p38，ERK1 / 2和JNK的SOD酶活性和磷酸化，并且在100μM时，可能通过MAPK和NF-κB信号通路对LPS诱导的氧化应激和炎症反应产生最大的抑制作用。