ArticleMolecular biology reports2023
Role of apoptosis and autophagy in mediating tramadol-induced neurodegeneration in the rat hippocampus.
Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- High-Altitude Hypoxia Activates JNK-p53 Signaling: Linking Hippocampal Energy Crisis to Cognitive Impairment.CNS neuroscience & therapeutics · 2026Article
- The mechanism of the JNK signaling pathway in drug addiction : Author list.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Ameliorative Effect of Vitamin C Against Tramadol-Induced Learning and Memory Impairment in Juvenile Rat Via Attenuation of Oxidative Stress and Dysfunctional Synaptic Plasticity.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Preventive Role of Simvastatin against Infertility: Potential Role of PGC-α/PPARβ/UCPs and NF-κβ Signaling Pathways.International journal of preventive medicine · 2025Review
- Unveiling the hidden dangers: a review of non-apoptotic programmed cell death in anesthetic-induced developmental neurotoxicity.Cell biology and toxicology · 2024Review
- Does Tramadol Exposure Have Unfavorable Effects on Hippocampus? A Review Study.Addiction & health · 2024Review
- Evaluation of histological and ultrastructural changes provoked by prenatal tramadol on postnatal cortical cerebellar neuronal development in rats: possible implication of Ki67, GFAP and MicroRNA-7/P53 signalling trajectories.Journal of molecular histology · 2024Article
- Minocycline Acts as a Neuroprotective Agent Against Tramadol-Induced Neurodegeneration: Behavioral and Molecular Evidence.International journal of preventive medicine · 2024Article
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTramadol (TRA) is an analgesic prescribed for treating mild to moderate pains, the abuse of which has increased in recent years. Chronic tramadol consumption produces neurotoxicity, although the mechanisms are unclear. The present study investigated the involvement of apoptosis and autophagy signaling pathways and the mitochondrial system in TRA-induced neurotoxicity. MATERIALS AND
methodsSixty adult male Wistar rats were divided into five groups that received standard saline or TRA in doses of 25, 50, 75, 100, or 150 mg/kg intraperitoneally for 21 days. On the 22nd day, the Open Field Test (OFT) was conducted. Jun N-Terminal Kinase (JNK), B-cell lymphoma-2 (Bcl-2), Beclin1, and Bcl-2-like protein 4 (Bax) proteins and tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) were measured in rat hippocampal tissue.
resultsTRA at doses 75, 100, and 150 mg/kg caused locomotor dysfunction in rats and increased total and phosphorylated forms of JNK and Beclin-1, Bax, and Caspase-3. TRA at the three higher doses also increased the phosphorylated (inactive) form of Bcl-2 level while decreasing the unphosphorylated (active) form of Bcl-2. Similarly, the protein levels of TNF-α and IL-1β were increased dose-dependently. The mitochondrial respiratory chain enzymes were reduced at the three higher doses of TRA.
conclusionTRA activated apoptosis and autophagy via modulation of TNF-α or IL-1β/JNK/Bcl-2/Beclin1 and Bcl-2/Bax signaling pathways and dysfunction of mitochondrial respiratory chain enzymes.
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