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Published on: August 15, 2012
Asperosaponin VI inhibits LPS-induced inflammatory response by activating PPAR-γ pathway in primary microglia
Jinqiang Zhang1, Saini Yi1, Chenghong Xiao1
1Guizhou University of Traditional Chinese Medicine, Guiyang 550025, China.
Abstract:
Microglia cells are the main mediators of neuroinflammation. Activation of microglia often aggravates the pathological process of various neurological diseases. Natural chemicals have unique advantages in inhibiting microglia-mediated neuroinflammation and improving neuronal function. Here, we examined the effects of asperosaponin VI (ASA VI) on LPS-activated primary microglia. Microglia were isolated from mice and pretreated with different doses of ASA VI, following lipopolysaccharide (LPS) administration. Activation and inflammatory response of microglia cells were evaluated by real-time fluorescence quantitative polymerase chain reaction (q-PCR), immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). Signaling pathways were detected by western blotting. We found that the ASA VI inhibited the morphological expansion of microglia cells, decreased the expression and release of proinflammatory cytokines, and promoted the expression of antiinflammatory cytokines in a dose-dependent manner. ASA VI also activated PPAR-γ signaling pathway in LPS-treated microglia. The anti-inflammatory effects of ASA VI in microglia were blocked by treating PPAR-γ antagonist (GW9662). These results showed that ASA VI promote the transition of microglia cells from proinflammatory to anti-inflammatory by regulating PPAR-γ pathway.
Insights
Asperosaponin VI (ASA VI) reduces neuroinflammation by inhibiting pro-inflammatory microglia. This natural compound shifts microglia to an anti-inflammatory state by activating the PPAR-γ pathway, offering therapeutic potential for neurological diseases.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia are key players in neuroinflammation, exacerbating neurological disease pathology.
- Natural compounds show promise in modulating microglia-mediated inflammation and enhancing neuronal function.
Purpose of the Study:
- To investigate the effects of asperosaponin VI (ASA VI) on lipopolysaccharide (LPS)-activated primary microglia.
- To determine the underlying molecular mechanisms, including the role of the PPAR-γ signaling pathway.
Main Methods:
- Primary mouse microglia were treated with varying doses of ASA VI followed by LPS stimulation.
- Microglia activation, cytokine expression (pro- and anti-inflammatory), and signaling pathways were assessed using q-PCR, ELISA, and Western blotting.
- The role of the PPAR-γ pathway was confirmed using a specific antagonist (GW9662).
Main Results:
- ASA VI inhibited microglia morphological activation and reduced the release of pro-inflammatory cytokines in a dose-dependent manner.
- ASA VI increased the expression of anti-inflammatory cytokines.
- Activation of the PPAR-γ signaling pathway by ASA VI was observed, and its blockade reversed the anti-inflammatory effects.
Conclusions:
- Asperosaponin VI effectively suppresses microglia-driven neuroinflammation.
- ASA VI promotes a shift from a pro-inflammatory to an anti-inflammatory microglia phenotype via the PPAR-γ pathway.
- These findings highlight ASA VI as a potential therapeutic agent for neurological disorders characterized by neuroinflammation.
