Peucedani Japonici Radix ameliorates lipopolysaccharide-induced neuroinflammation by regulating microglial responses. (1st November 2018)

• Record Type: Journal Article
• Authors: Ju, In Gyoung; Choi, Jin Gyu; Kim, Namkwon; Kwak, Chaewon; Lee, Jong Kil; Oh, Myung Sook
• Is Part Of: Neuroscience letters. Volume 686(2018)
• Page Start: 161
• Page End: 167
• Publication Date: 2018-11-01
• Subjects: Microglia -- Neuroinflammation -- Nuclear factor kappa B -- Peucedani Japonici Radix; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2018.09.010
• Languages: English
• ISSNs: 0304-3940

Abstract

Graphical abstract: Highlights: PJR inhibited LPS-induced increase of pro-inflammatory mediators. PJR regulated microglial responses via inhibiting NF-kB translocation into nuclear. PJR suppressed LPS-induced microglial activation in mouse brain. Abstract: Neuroinflammation is an inflammatory process within the central nervous system that is mediated by microglial activation, which releases pro-inflammatory mediators leading to neurodegeneration. In this study, we investigated the effects of Peucedani Japonici Radix (PJR), a medicinal herb traditionally used in East Asia to treat neuroinflammation both in vitro and in vivo . First, we examined the effects of PJR on pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. The results showed that PJR suppressed the LPS-induced increase of several inflammatory factors, such as nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, prostaglandin E2, interleukin-1β, and tumor necrosis factor-α. We also revealed that PJR inhibited the nuclear factor kappa B (NF-κB) pathway, which is the upstream modulator of inflammatory processes. Furthermore, to confirm the regulatory effects of PJR on microglia in vivo, we measured the number of ionized calcium-binding adapter molecule 1-positive cells in mouse brains and found that PJR treatment reduced microglial activation. Taken together, these results suggest that PJR inhibits microglia-mediated neuroinflammation through the modulation of NF-κB signaling and has the therapeutic potential to prevent inflammation-related neurodegenerative diseases.