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.

Jing Zhang, Na Song, Yuzhi Liu, Junwei Guo
Author Information
  1. Jing Zhang: Nursing Department, Aviation General Hospital, Beijing, 100012, China.
  2. Na Song: Second Ward, Binzhou Youfu Hospital of Shandong Province, Binzhou, 256600, Shandong, China.
  3. Yuzhi Liu: Female Ward, Binzhou Youfu Hospital of Shandong Province, Binzhou, 256600, Shandong, China.
  4. Junwei Guo: Psychological Outpatient Department, Chongqing Traditional Chinese Medicine Hospital, Chongqing, 404000, China. junweiguo01@163.com.

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.

Keywords

References

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MeSH Term

Amyloid beta-Peptides
Animals
Cell Line
Cell Survival
Gene Knockdown Techniques
Heme Oxygenase-1
Inflammation
Membrane Proteins
Mice
NF-E2-Related Factor 2
NF-kappa B p50 Subunit
Oxidative Stress
Peptide Fragments
Saponins
Signal Transduction
Toll-Like Receptor 4
Triterpenes

Chemicals

Amyloid beta-Peptides
Membrane Proteins
NF-E2-Related Factor 2
NF-kappa B p50 Subunit
Nfe2l2 protein, mouse
Peptide Fragments
Saponins
Tlr4 protein, mouse
Toll-Like Receptor 4
Triterpenes
amyloid beta-protein (1-42)
Nfkb1 protein, mouse
platycodin D
Heme Oxygenase-1
Hmox1 protein, mouse

Word Cloud

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