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Rhynchophylline attenuates LPS-induced pro-inflammatory responses through down-regulation of MAPK/NF-κB signaling
Yu Song1, Rong Qu, Shenghua Zhu
1Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, PR China.
Abstract:
Excessive activation of microglial cells has been implicated in various types of neuroinflammation. Suppression of microglial activation would have therapeutic benefits, leading to the alleviation of the progression of neurodegeneration. In this study, the inhibitory effects of rhynchophylline (RIN), a tetracyclic oxindole alkaloid component isolated from Uncaria rhynchophylla (Miq.) Jacks., on the production of pro-inflammatory mediators were investigated in lipopolysaccharide (LPS)-stimulated microglia. The results showed that RIN markedly reduced the production of nitric oxide (NO), prostaglandins E(2) (PGE(2) ), monocyte chemoattractant protein (MCP-1), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in LPS-activated microglia. The mRNA expression levels of iNOS and COX-2 were also depressed by RIN in a concentration-dependent manner. Further studies revealed that RIN blocked IκBα phosphorylation and degradation, inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs). In summary, these data suggest that RIN suppresses inflammatory responses of microglia and may act as a potential therapeutic agent for various neurodegenerative diseases involving neuroinflammation.
Insights
Rhynchophylline (RIN) suppresses the activation of microglial cells, reducing key inflammatory mediators involved in neuroinflammation. This suggests RIN may be a potential therapeutic for neurodegenerative diseases.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Microglial cell activation is central to neuroinflammation and neurodegeneration.
- Targeting microglial activation offers therapeutic potential for neurodegenerative diseases.
Purpose of the Study:
- To investigate the inhibitory effects of rhynchophylline (RIN) on pro-inflammatory mediator production in lipopolysaccharide (LPS)-stimulated microglia.
- To explore RIN's potential as a therapeutic agent for neuroinflammation.
Main Methods:
- Investigated RIN's effects on nitric oxide (NO), prostaglandins E(2) (PGE(2)), monocyte chemoattractant protein (MCP-1), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) production.
- Assessed mRNA expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2).
- Examined the impact of RIN on IκBα phosphorylation/degradation and mitogen-activated protein kinases (MAPKs) phosphorylation.
Main Results:
- RIN significantly reduced the production of NO, PGE(2), MCP-1, TNF-α, and IL-1β in LPS-activated microglia.
- RIN dose-dependently decreased iNOS and COX-2 mRNA expression.
- RIN inhibited IκBα phosphorylation and degradation, and suppressed MAPK phosphorylation.
Conclusions:
- Rhynchophylline effectively suppresses inflammatory responses in microglia.
- RIN demonstrates potential as a therapeutic agent for neurodegenerative diseases associated with neuroinflammation.