Antineuroinflammatory Effects of Modified Wu-Zi-Yan-Zong Prescription in β-Amyloid-Stimulated BV2 Microglia via the NF-κB and ERK/p38 MAPK Signaling Pathways.
Qian YuFang-Jiao SongJin-Feng ChenXin DongYong JiangKe-Wu ZengPeng-Fei TuXue-Mei WangPublished in: Evidence-based complementary and alternative medicine : eCAM (2017)
Modified Wu-Zi-Yan-Zong prescription (MWP), a traditional Chinese medicinal decoction, has possessed the neuroprotective and anti-inflammatory properties. The mechanisms associated with these properties, however, are not completely understood. We designed the experiments to elucidate the antineuroinflammatory property of MWP in BV2 microglia activated by β-amyloid (Aβ), which is a characteristic feature of Alzheimer's disease (AD). The composition of MWP was studied using HPLC. BV2 microglia cells were then treated with Aβ in the presence or absence of MWP. The effects of MWP treatment on Aβ-activated neuroinflammation were determined using PCR, western blotting, and immunofluorescence staining. MWP significantly inhibited the mRNA expression of inflammatory mediators such as IL-1β, IL-6, TNF-α, and MCP-1, as well as the expression of inducible nitric oxide synthase (iNOS) in Aβ-activated BV2 microglia. MWP also inhibited the nuclear translocation and signaling pathway of nuclear factor kappa B (NF-κB) by suppressing inhibitor of nuclear factor-κB (IκB) degradation and downregulating IκB kinase β (IKKβ) phosphorylation. Moreover, MWP decreased extracellular regulated protein kinase (ERK)/p38 mitogen-activated protein kinase (MAPK) phosphorylation, which is an important signaling pathway for proinflammatory gene expression. We concluded that MWP could suppress neuroinflammatory responses in Aβ-activated BV2 microglia via the NF-κB and ERK/p38 MAPK signaling cascades and could prove an effective therapeutic agent for the prevention and treatment of neuroinflammatory diseases such as AD.
Keyphrases
- signaling pathway
- nuclear factor
- inflammatory response
- lps induced
- toll like receptor
- lipopolysaccharide induced
- pi k akt
- induced apoptosis
- protein kinase
- nitric oxide synthase
- cell cycle arrest
- epithelial mesenchymal transition
- gene expression
- neuropathic pain
- anti inflammatory
- rheumatoid arthritis
- machine learning
- cell proliferation
- cell death
- south africa
- oxidative stress
- immune response
- traumatic brain injury
- transcription factor
- spinal cord
- tandem mass spectrometry
- cerebral ischemia
- binding protein
- tyrosine kinase
- newly diagnosed
- cognitive impairment
- smoking cessation
- solid phase extraction