Abstract:
:Through searching for anti‑neuroinflammatory metabolites from Nardostachys jatamansi extracts, nardostachin was revealed to exert anti‑neuroinflammatory effects against lipopolysaccharide (LPS)‑induced overproduction of nitric oxide and prostaglandin E2 in BV2 and rat primary microglial cells. Furthermore, nardostachin inhibited the production of inducible nitric oxide synthase and cyclooxygenase‑2 as well as pro‑inflammatory cytokines, including interleukin (IL)‑1β, IL‑6, IL‑12 and tumor necrosis factor‑α in LPS‑stimulated BV2 and rat primary microglial cells. In a mechanistic study, nardostachin exhibited inhibitory activity on the nuclear factor (NF)‑κB signaling pathway in LPS‑stimulated BV2 and rat primary microglial cells by repressing IκB‑α phosphorylation and blocking NF‑κB translocation. Furthermore, nardostachin exhibited inhibitory effects on LPS‑induced phosphorylation of c‑Jun N‑terminal kinase (JNK) mitogen‑activated protein kinase (MAPK). Additionally, nardostachin repressed protein expression of Toll‑like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) in LPS‑induced BV2 and rat primary microglial cells. These results suggested that nardostachin exerts anti‑neuroinflammatory effects on LPS‑induced BV2 and rat primary microglial cells by suppressing the TLR4‑MyD88‑NF‑κB and JNK MAPK pathways.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Kim DC,Park JS,Yoon CS,Kim YC,Oh Hdoi
10.3892/mmr.2020.11720subject
Has Abstractpub_date
2021-01-01 00:00:00issue
1eissn
1791-2997issn
1791-3004pii
82journal_volume
23pub_type
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