ArticleMolecular neurobiology2025
Tetramethylpyrazine-caffeic Acid Hybrid CT-011 Exerts Dopaminergic Neuroprotection Through Inhibiting Microglia-mediated Neuroinflammation.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Parkinson's disease (PD) is the second most prevalent neurological disorder without a clear etiology and specific cure. Microglia-mediated neuroinflammation plays a pivotal role in the pathogenesis and progression of PD, which is influenced by various factors and involves multiple signaling pathways. CT-011, synthesized by combining nitrone-tetramethyl pyrazine (TMP) and caffeic acid through an ester bond, has shown neuroprotection against ischemic stroke and glutamate-induced neuronal damage in animal models. The purpose of this study is to explore the impact of CT-011 on PD-related neuroinflammation and its potential in treating PD. Results showed that CT-011 significantly inhibited lipopolysaccharide (LPS)-induced release of pro-inflammatory cytokines and mediators in BV2 microglial cells. CT-011 also effectively mitigated LPS-induced mitochondrial membrane potential (MMP) reduction, mitochondrial and intracellular reactive oxygen species (ROS) production. Meanwhile, CT-011's anti-inflammatory effect was related to its inhibition of the TLR4-mediated MyD88/NF-B and PI3K-mediated AKT/GSK3β pathways. More significantly, CT-011 repressed the NLRP3 inflammasome activation. Additionally, CT-011 protected primary neurons against microglial-mediated neurotoxicity in vitro, and ameliorated dopaminergic neuronal damage in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice with a consistent anti-neuroinflammatory effect in vivo. These results demonstrate that CT-011 effectively inhibits microglia-mediated neuroinflammation and exerts neuroprotective effects on dopamine neurons, thus making it a promising therapeutic candidate for PD.
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