ArticleMolecular neurobiology2018
Cyclooxygenase-2 Directs Microglial Activation-Mediated Inflammation and Oxidative Stress Leading to Intrinsic Apoptosis in Zn-Induced Parkinsonism.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 21 citations in OpenAlex.
- Zinc homeostasis imbalance: Potential therapeutic value in neurodegenerative diseases.Neural regeneration research · 2026Article
- Zinc in psychosis (Review).Molecular medicine reports · 2025Review
- From Fundamentals to Innovation in Alzheimer's Disease: Molecular Findings and Revolutionary Therapies.International journal of molecular sciences · 2024Review
- Heavy Metal Mediated Progressive Degeneration and Its Noxious Effects on Brain Microenvironment.Biological trace element research · 2024Review
- TXNIP/NLRP3 aggravates global cerebral ischemia-reperfusion injury-induced cognitive decline in mice.Heliyon · 2024Article
- Brain oxidative stress mediates anxiety-like behavior induced by indomethacin in zebrafish: protective effect of alpha-tocopherol.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Emphasizing the Crosstalk Between Inflammatory and Neural Signaling in Post-traumatic Stress Disorder (PTSD).Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Review
- Tempol and silymarin rescue from zinc-induced degeneration of dopaminergic neurons through modulation of oxidative stress and inflammation.Molecular and cellular biochemistry · 2023Article
- Postnatal zinc or paraquat administration increases paraquat or zinc-induced loss of dopaminergic neurons: insight into augmented neurodegeneration.Molecular and cellular biochemistry · 2020Article
- The Underlying Mechanism ofFrontiers in pharmacology · 2020Article
- Inhibition of glutathione S-transferase-pi triggers c-jun N-terminal kinase-dependent neuronal death in Zn-induced Parkinsonism.Molecular and cellular biochemistry · 2019Article
- Neuroprotective Effect of Optimized Yinxieling Formula in 6-OHDA-Induced Chronic Model of Parkinson's Disease through the Inflammation Pathway.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Artemisinin Prevents Glutamate-Induced Neuronal Cell Death Via Akt Pathway Activation.Frontiers in cellular neuroscience · 2018Article
- Article
- Autologous Adipose-Derived Stem Cells Reduce Burn-Induced Neuropathic Pain in a Rat Model.International journal of molecular sciences · 2017Article
- COX-2 metabolic products, the prostaglandin IOncotarget · 2017Article
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4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is decisive in zinc (Zn)-induced nigrostriatal dopaminergic neurodegeneration; however, the contribution of cyclooxygenase-2 (COX-2) is not yet known. The present study aimed to explore the role of COX-2 in Zn-induced Parkinsonism and its association with the microglial activation. Male Wistar rats were treated intraperitoneally (i.p.) with Zn as zinc sulphate (20 mg/kg) along with respective controls for 2-12 weeks. In a few sets, animals were also treated with/without celecoxcib (CXB, 20 mg/kg, i.p.), a selective COX-2 inhibitor. Indexes of the nigrostriatal neurodegeneration, oxidative stress, inflammation and apoptosis were measured in the animals/nigrostriatal tissue. Zn induced time-dependent increase in the expression of COX-2 while COX-1 expression was unaltered. Zn reduced the neurobehavioral activities, striatal dopamine content, tyrosine hydroxylase (TH) expression and number of dopaminergic neurons. While oxidative stress; microglial activation; expression of microglial cell surface marker-CD11b; cytochrome c release; caspase-9/3 activation; level of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 and Bcl-2-associated protein x (Bax) translocation from the cytosol to mitochondria were induced in the Zn-treated group, expression of B-cell lymphoma-2 (Bcl-2) was found to be reduced. CXB significantly attenuated Zn-induced increase in COX-2 expression and restored TH-expression, dopamine content, level of inflammatory cytokines and neurobehavioral indexes towards normalcy. Moreover, CXB also attenuated Zn-induced increase in microglial activation, oxidative stress and apoptotic markers towards normal levels. Results of the study thus demonstrate that COX-2 induces microglial activation that provokes the release of inflammatory mediators, which in turn augments oxidative stress and intrinsic apoptosis leading to dopaminergic neurodegeneration in Zn-induced Parkinsonism.
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