Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Ochang-eup, Cheongwon-gu, Cheongju-si, Chungcheongbuk-do 28116, Republic of Korea.
International Biological Material Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Yuseong-gu, Daejeon 34141, Republic of Korea.
Int J Mol Med. 2018 Jun;41(6):3709-3716. doi: 10.3892/ijmm.2018.3559. Epub 2018 Mar 12.
Passiflora foetida L. (Passifloraceae), a perennial climber in general, is used for treating many ailments in conventional medicine. In this study, the anti-inflammatory effect of methanolic extracts of P. foetida L. (PFME) and the involvement of nuclear factor-κB (NF-κB) signalling in the regulation of inflammation were investigated. PFME prevented the production of prostaglandin E2 (PGE2) and the expression of inducible cyclooxygenase-2 (COX-2) in lipopolysaccharide (LPS)-induced macrophage cells. Additionally, PFME reduced the release of pro-inflammatory cytokines. Moreover, in LPS-induced RAW264.7 cells, the phosphorylation of MAPKs (ERK1/2, p38 and JNK) was suppressed by PFME. Furthermore, PFME inhibited the NF-κB activation induced by LPS, which was associated with nuclear p65 levels with the abrogation of IκBα degradation and subsequent decreases. These results indicated that the PFME inhibited the LPS-induced inflammatory and oxidative responses. Therefore, we propose that the PFME may be therapeutic for treating inflammatory diseases.
西番莲（西番莲科）是一种多年生攀缘植物，在传统医学中被用于治疗多种疾病。本研究旨在探讨西番莲甲醇提取物（PFME）的抗炎作用及其对核因子-κB（NF-κB）信号通路的调控作用。结果表明，PFME 可抑制脂多糖（LPS）诱导的巨噬细胞中环氧化酶-2（COX-2）的表达和前列腺素 E2（PGE2）的产生，减少促炎细胞因子的释放。此外，PFME 还可抑制 LPS 诱导的 RAW264.7 细胞中丝裂原活化蛋白激酶（MAPKs）（ERK1/2、p38 和 JNK）的磷酸化。同时，PFME 可抑制 LPS 诱导的 NF-κB 激活，这与核 p65 水平的降低有关，同时还可阻断 IκBα 的降解。综上所述，PFME 可抑制 LPS 诱导的炎症和氧化应激反应。因此，我们推测 PFME 可能具有治疗炎症性疾病的潜力。
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