Department of Acupuncture and Moxibustion, Dongeui University College of Oriental Medicine, Busan, Republic of Korea.
Int J Mol Med. 2013 Jun;31(6):1357-66. doi: 10.3892/ijmm.2013.1330. Epub 2013 Apr 4.
Radix platycodi is the root of Platycodon grandiflorus A. DC, which has been widely used as a food material and for the treatment of a number of chronic inflammatory diseases in traditional oriental medicine. In this study, the anti‑inflammatory effects of the saponins isolated from radix platycodi (PGS) on the production of inflammatory mediators and cytokines in lipopolysaccharide (LPS)-stimulated BV2 murine microglial cells were examined. We also investigated the effects of PGS on LPS‑induced nuclear factor‑κB (NF-κB) activation and phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) signaling pathways. Following stimulation with LPS, elevated nitric oxide (NO), prostaglandin E2 (PGE2) and pro-inflammatory cytokine production was detected in the BV2 microglial cells. However, PGS significantly inhibited the excessive production of NO, PGE2 and pro‑inflammatory cytokines, including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in a concentration-dependent manner without causing any cytotoxic effects. In addition, PGS suppressed NF-κB translocation and inhibited the LPS-induced phosphorylation of AKT and MAPKs. Our results indicate that the inhibitory effect of PGS on LPS-stimulated inflammatory response in BV2 microglial cells is associated with the suppression of NF-κB activation and the PI3K/AKT and MAPK signaling pathways. Therefore, these findings suggest that PGS may be useful in the treatment of neurodegenerative diseases by inhibiting inflammatory responses in activated microglial cells.
桔梗根是桔梗(Platycodon grandiflorus A. DC)的根,在传统东方医学中,它被广泛用作食品材料和治疗多种慢性炎症性疾病。在这项研究中,我们研究了从桔梗中分离得到的皂苷(PGS)对脂多糖(LPS)刺激的 BV2 小鼠小胶质细胞中炎症介质和细胞因子产生的抗炎作用。我们还研究了 PGS 对 LPS 诱导的核因子-κB(NF-κB)激活以及磷酸肌醇 3-激酶(PI3K)/蛋白激酶 B(AKT)和丝裂原活化蛋白激酶(MAPK)信号通路的影响。在 LPS 刺激后,BV2 小胶质细胞中检测到一氧化氮(NO)、前列腺素 E2(PGE2)和促炎细胞因子的产生增加。然而,PGS 能够以浓度依赖的方式显著抑制过量的 NO、PGE2 和促炎细胞因子(包括白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α))的产生,而没有产生任何细胞毒性作用。此外,PGS 抑制 NF-κB 易位并抑制 LPS 诱导的 AKT 和 MAPKs 磷酸化。我们的结果表明,PGS 对 LPS 刺激的 BV2 小胶质细胞炎症反应的抑制作用与抑制 NF-κB 激活以及 PI3K/AKT 和 MAPK 信号通路有关。因此,这些发现表明 PGS 可能通过抑制激活的小胶质细胞中的炎症反应,在治疗神经退行性疾病方面具有应用价值。