Platycodin D Inhibits β-Amyloid-Induced Inflammation and Oxidative Stress in BV-2 Cells Via Suppressing TLR4/NF-κB Signaling Pathway and Activating Nrf2/HO-1 Signaling Pathway.

Abstract

Alzheimer's disease (AD) is a common neurodegenerative disease associated with deposition of β-amyloid peptide (Aβ). Platycodin D (PLD), a triterpenesaponin, may possess neuro-protective effect. In the current study, we aimed to explore the effects of PLD on Aβ-induced inflammation and oxidative stress in microglial BV-2 cells. Our study showed that PLD treatment improved cell viability in Aβ-induced BV-2 cells. PLD attenuated Aβ-induced inflammation with deceased production of TNF-α, IL-1β and IL-6 in Aβ-induced BV-2 cells. PLD also mitigated the oxidative stress in Aβ-induced BV-2 cells, as evidenced by deceased production of ROS and MDA, and increased SOD activity. Furthermore, the increased expression levels of TLR4 and p-p65 and decreased IκBα expression in the Aβ-stimulated BV-2 cells were attenuated by PLD treatment. Overexpression of TLR4 reversed the anti-inflammatory effect of PLD in Aβ-stimulated BV-2 cells. In addition, PLD treatment enhanced the Aβ-stimulated increase in the expression levels of Nrf2, HO-1, and NQO1 in BV-2 cells. Knockdown of Nrf2 abrogated the anti-oxidative effect of PLD in Aβ-stimulated BV-2 cells. In conclusion, these findings indicated that PLD protected BV-2 cells from Aβ-induced oxidative stress and inflammation via regulating the TLR4/NF-κB and Nrf2/HO-1 signaling pathways. Thus, PLD may be a potential candidate for the treatment of AD.