ArticleMolecular neurobiology2016
Minocycline Rescues from Zinc-Induced Nigrostriatal Dopaminergic Neurodegeneration: Biochemical and Molecular Interventions.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- Postnatal Exposure Sensitizes for Zinc/Paraquat-Induced Neuronal Apoptosis, Adulthood Exposure Leads to the Final Effects.Journal of molecular neuroscience : MN · 2026Article
- Metallothioneins in Neurodegenerative Diseases: Metal Homeostasis, Autoimmunity, and Therapeutic Potential.Molecular neurobiology · 2026Review
- An update on the involvement of inflammatory mediators in Parkinson's disease pathogenesis.Archives of toxicology · 2025Review
- Zinc-Dependent Modulation of Dopamine Release and Uptake Is Altered in Parkinson's Disease Model Zebrafish.ACS chemical neuroscience · 2025Article
- Impaired Mitochondrial Function and Ubiquitin Proteasome System Activate α-Synuclein Aggregation in Zinc-Induced Neurotoxicity: Effect of Antioxidants.Journal of molecular neuroscience : MN · 2025Article
- Engineered bio-functional material-based nerve guide conduits for optic nerve regeneration: a view from the cellular perspective, challenges and the future outlook.Regenerative biomaterials · 2025Review
- Minocycline as a prospective therapeutic agent for cancer and non-cancer diseases: a scoping review.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Evaluating Manganese, Zinc, and Copper Metal Toxicity on SH-SY5Y Cells in Establishing an Idiopathic Parkinson's Disease Model.International journal of molecular sciences · 2023Article
- Tempol and silymarin rescue from zinc-induced degeneration of dopaminergic neurons through modulation of oxidative stress and inflammation.Molecular and cellular biochemistry · 2023Article
- Minocycline Protects PC12 Cells Against Cadmium-Induced Neurotoxicity by Modulating Apoptosis.Biological trace element research · 2023Article
- Zinc Homeostasis: An Emerging Therapeutic Target for Neuroinflammation Related Diseases.Biomolecules · 2023Review
- The Interplay between Gut Microbiota and Parkinson's Disease: Implications on Diagnosis and Treatment.International journal of molecular sciences · 2022Review
- Retinal Ganglion Cell Survival and Axon Regeneration after Optic Nerve Injury: Role of Inflammation and Other Factors.International journal of molecular sciences · 2022Review
- Early Life Social Stress Causes Sex- and Region-Dependent Dopaminergic Changes that Are Prevented by Minocycline.Molecular neurobiology · 2022Article
- Mitochondrial Dysfunction Contributes To Zinc-induced Neurodegeneration: a Link with NADPH Oxidase.Journal of molecular neuroscience : MN · 2022Article
- Zinc antagonizes iron-regulation of tyrosine hydroxylase activity and dopamine production in Drosophila melanogaster.BMC biology · 2021Article
- A Characterization of the Effects of Minocycline Treatment During Adolescence on Structural, Metabolic, and Oxidative Stress Parameters in a Maternal Immune Stimulation Model of Neurodevelopmental Brain Disorders.The international journal of neuropsychopharmacology · 2021Article
- Synaptic Zinc: An Emerging Player in Parkinson's Disease.International journal of molecular sciences · 2021Review
- Microglial Activation Mediates Noradrenergic Locus Coeruleus Neurodegeneration via Complement Receptor 3 in a Rotenone-Induced Parkinson's Disease Mouse Model.Journal of inflammation research · 2021Article
- Zinc.Advances in food and nutrition research · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of zinc (Zn) in dopaminergic neurons is implicated in Parkinson's disease (PD), and microglial activation plays a critical role in toxin-induced Parkinsonism. Oxidative stress is accused in Zn-induced dopaminergic neurodegeneration; however, its connection with microglial activation is still not known. This study was undertaken to elucidate the role and underlying mechanism of microglial activation in Zn-induced nigrostriatal dopaminergic neurodegeneration. Male Wistar rats were treated intraperitoneally with/without zinc sulphate (20 mg/kg) in the presence/absence of minocycline (30 mg/kg), a microglial activation inhibitor, for 2-12 weeks. While neurobehavioral and biochemical indexes of PD and number of dopaminergic neurons were reduced, the number of microglial cells was increased in the substantia nigra of the Zn-exposed animals. Similarly, Zn elevated lipid peroxidation (LPO) and activities of superoxide dismutase (SOD) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase; however, catalase activity was reduced. Besides, Zn increased an association of NADPH oxidase subunit p67(phox) with membrane, cytochrome c release from the mitochondria and cleavage of pro-caspase 3. Zn attenuated the expression of tyrosine hydroxylase (TH) and vesicular monoamine transporter-2 (VMAT-2) while augmented the expression of dopamine transporter (DAT) and heme oxygenase-1 (HO-1). Minocycline alleviated Zn-induced behavioural impairments, loss of TH-positive neurons, activated microglial cells and biochemical indexes and modulated the expression of studied genes/proteins towards normalcy. The results demonstrate that minocycline reduces the number of activated microglial cells and oxidative stress, which rescue from Zn-induced changes in the expression of monoamine transporter and nigrostriatal dopaminergic neurodegeneration.
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Registered trials
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