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month download article/chapter jnk-sp1-dj-1 axis activation neurotoxin-induced animal models jnk-sp1-dj-1 pathway promote mitophagy-mediated neuroprotection randomized delayed-start trial trpm2 channel-mediated regulation jnk-sp1-dj-1 axis pi3k/akt/mtor pathway mitochondria-specific drug release stress-specific jnk activity shih-ya hung 1-methyl-4-phenylpyridinium-induced autophagy chien-hsing lee full article pdf oleanolic acid protects pharmacal research aims jnk-signaling pathway jnk pathway signaling privacy choices/manage cookies sp1-dependent activation lipid-lowering effects oleanolic acid activates hsueh-shih road mitophagy-driven neuroprotection electroacupuncture promotes recovery accepted manuscript version dj-1 activates mitophagy cancer cell survival human dj-1 promoter creation research center ros-dependent regulation induced cellular model induced mouse model article archives induced dj-1 expression article yang mitophagic protein dj-1 attenuating intracellular ros striatal microglial activation jnk transduction pathways preclinical animal model china medical university mouse dj-1 genes holds exclusive rights neural cell lines activates latent parkin neuronal pc12 cells mitochondrial quality control reduced neuronal death

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         headline:Oleanolic acid activates the JNK-Sp1-DJ-1 axis to promote mitophagy-mediated neuroprotection in dopaminergic neurons for Parkinson’s disease treatment
         description:Parkinson’s disease (PD) is a prevalent neurodegenerative disorder marked by mitochondrial dysfunction and oxidative stress. Although levodopa remains the gold standard for managing PD motor symptoms, it lacks neuroprotective and disease-modifying effects, highlighting the need for new neuroprotective therapies. Mitophagy, the selective mitochondrial degradation by autophagy, is critical for neuronal health. Oleanolic acid, a natural hepatoprotective compound, shows uncertain efficacy in PD treatment. This study investigated the neuroprotective effects and underlying mechanisms of oleanolic acid using the 1-methyl-4-phenylpyridinium (MPP⁺)-induced cellular model and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. In vitro, oleanolic acid demonstrated dopaminergic neuroprotection by reducing mitochondrial dysfunction and reactive oxygen species accumulation in PD cells. It upregulated the mitophagic protein DJ-1, enhancing the sequestration of damaged mitochondria into autophagosomes by mitophagy. DJ-1 knockdown attenuated oleanolic acid’s neuroprotection, confirming DJ-1’s role in oleanolic acid’s action. In vivo, pre-treatment with oleanolic acid in MPTP-induced PD mice prevented PD-like motor symptoms, reduced neuronal death in the substantia nigra, and mitigated striatal neurodegeneration. Post-treatment with oleanolic acid not only reduced these effects but also increased Bcl-2 and DJ-1 levels in the substantia nigra and striatum. In vitro, oleanolic acid activated JNK for Sp1 upregulation and nuclear translocation, which induced DJ-1 expression. Computational modeling predicted that oleanolic acid likely interacts with JNK, suggesting this binding might be necessary for JNK-Sp1-DJ-1 axis activation for mitophagy-driven neuroprotection. These results highlight oleanolic acid’s potential as a therapeutic agent in PD prevention and treatment via the JNK-Sp1-DJ-1 pathway. Further studies are required to validate its efficacy.
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      headline:Oleanolic acid activates the JNK-Sp1-DJ-1 axis to promote mitophagy-mediated neuroprotection in dopaminergic neurons for Parkinson’s disease treatment
      description:Parkinson’s disease (PD) is a prevalent neurodegenerative disorder marked by mitochondrial dysfunction and oxidative stress. Although levodopa remains the gold standard for managing PD motor symptoms, it lacks neuroprotective and disease-modifying effects, highlighting the need for new neuroprotective therapies. Mitophagy, the selective mitochondrial degradation by autophagy, is critical for neuronal health. Oleanolic acid, a natural hepatoprotective compound, shows uncertain efficacy in PD treatment. This study investigated the neuroprotective effects and underlying mechanisms of oleanolic acid using the 1-methyl-4-phenylpyridinium (MPP⁺)-induced cellular model and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. In vitro, oleanolic acid demonstrated dopaminergic neuroprotection by reducing mitochondrial dysfunction and reactive oxygen species accumulation in PD cells. It upregulated the mitophagic protein DJ-1, enhancing the sequestration of damaged mitochondria into autophagosomes by mitophagy. DJ-1 knockdown attenuated oleanolic acid’s neuroprotection, confirming DJ-1’s role in oleanolic acid’s action. In vivo, pre-treatment with oleanolic acid in MPTP-induced PD mice prevented PD-like motor symptoms, reduced neuronal death in the substantia nigra, and mitigated striatal neurodegeneration. Post-treatment with oleanolic acid not only reduced these effects but also increased Bcl-2 and DJ-1 levels in the substantia nigra and striatum. In vitro, oleanolic acid activated JNK for Sp1 upregulation and nuclear translocation, which induced DJ-1 expression. Computational modeling predicted that oleanolic acid likely interacts with JNK, suggesting this binding might be necessary for JNK-Sp1-DJ-1 axis activation for mitophagy-driven neuroprotection. These results highlight oleanolic acid’s potential as a therapeutic agent in PD prevention and treatment via the JNK-Sp1-DJ-1 pathway. Further studies are required to validate its efficacy.
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         JNK-Sp1 pathway
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         Parkinson’s disease
         Pharmacy
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