ArticleMolecular medicine reports2021
The antidiabetic drug troglitazone protects against PrP (106‑126)‑induced neurotoxicity via the PPARγ‑autophagy pathway in neuronal cells.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Troglitazone Reduction of Intracellular Mycobacterium tuberculosis Survival Via Macrophage Autophagy Through LKB1-AMPKα Signaling.The Journal of infectious diseases · 2025Article
- Unveiling the shield: Troglitazone's impact on epilepsy-induced nerve injury through ferroptosis inhibition.CNS neuroscience & therapeutics · 2024Article
- Research progress of coumarins and their derivatives in the treatment of diabetes.Journal of enzyme inhibition and medicinal chemistry · 2022Review
- Cross-Linking Cellular Prion Protein Induces Neuronal Type 2-Like Hypersensitivity.Frontiers in immunology · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases, which involve the alteration of cellular prion protein into a misfolded isoform, disrupt the central nervous systems of humans and animals alike. Prior research has suggested that peroxisome proliferator‑activator receptor (PPAR)γ and autophagy provide some protection against neurodegeneration. PPARs are critical to lipid metabolism regulation and autophagy is one of the main cellular mechanisms by which cell function and homeostasis is maintained. The present study examined the effect of troglitazone, a PPARγ agonist, on autophagy flux in a prion peptide (PrP) (106‑126)‑mediated neurodegeneration model. Western blot analysis confirmed that treatment with troglitazone increased LC3‑II and p62 protein expression, whereas an excessive increase in autophagosomes was verified by transmission electron microscopy. Troglitazone weakened PrP (106‑126)‑mediated neurotoxicity via PPARγ activation and autophagy flux inhibition. A PPARγ antagonist blocked PPARγ activation as well as the neuroprotective effects induced by troglitazone treatment, indicating that PPARγ deactivation impaired troglitazone‑mediated protective effects. In conclusion, the present study demonstrated that troglitazone protected primary neuronal cells against PrP (106‑126)‑induced neuronal cell death by inhibiting autophagic flux and activating PPARγ signals. These results suggested that troglitazone may be a useful therapeutic agent for the treatment of neurodegenerative disorders and prion diseases.
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