| Title | Antineuroinflammatory Effects of Modified Wu-Zi-Yan-Zong Prescription in beta-Amyloid-Stimulated BV2 Microglia via the NF-kappa B and ERK/p38 MAPK Signaling Pathways |
| Authors | Yu, Qian Song, Fang-Jiao Chen, Jin-Feng Dong, Xin Jiang, Yong Zeng, Ke-Wu Tu, Peng-Fei Wang, Xue-Mei |
| Affiliation | Peking Univ, Hosp 1, Res Studio Integrat Tradit & Western Med, Beijing 100034, Peoples R China. Peking Univ, Sch Pharmaceut Sci, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China. Peking Univ, Hosp 1, Res Studio Integrat Tradit & Western Med, Beijing 100034, Peoples R China. Zeng, KW Tu, PF (reprint author), Peking Univ, Sch Pharmaceut Sci, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China. |
| Keywords | ALZHEIMERS-DISEASE NEUROINFLAMMATION ACTIVATION CELLS JNK INFLAMMATION DYSFUNCTION MECHANISMS |
| Issue Date | 2017 |
| Publisher | EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE |
| Citation | EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE.2017. |
| Abstract | 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 beta-amyloid (A beta), 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 A beta in the presence or absence of MWP. The effects of MWP treatment on A beta-activated neuroinflammation were determined using PCR, western blotting, and immunofluorescence staining. MWP significantly inhibited the mRNA expression of inflammatory mediators such as IL-1 beta, IL-6, TNF-alpha, and MCP-1, as well as the expression of inducible nitric oxide synthase (iNOS) in A beta-activated BV2 microglia. MWP also inhibited the nuclear translocation and signaling pathway of nuclear factor kappa B (NF-kappa B) by suppressing inhibitor of nuclear factor-kappa B (I kappa B)degradation and downregulating I kappa B kinase beta (IKK beta.) 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 A beta-activated BV2 microglia via the NF-kappa B and ERK/p38 MAPK signaling cascades and could prove an effective therapeutic agent for the prevention and treatment of neuroinflammatory diseases such as AD. |
| URI | http://hdl.handle.net/20.500.11897/475920 |
| ISSN | 1741-427X |
| DOI | 10.1155/2017/8470381 |
| Indexed | SCI(E) |
| Appears in Collections: | 第一医院 药学院 天然药物与仿生药物国家重点实验室 |
