ArticleMolecular biology reports2020
Minocycline attenuates depressive-like behaviors in mice treated with the low dose of intracerebroventricular streptozotocin; the role of mitochondrial function and neuroinflammation.
Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 26 citations in OpenAlex.
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- Protective role of fucoidan against cognitive deficits and redox imbalance in a scopolamine-induced Alzheimer's disease model in rats.Scientific reports · 2025Article
- Minocycline Treatment Improves Memory and Reduces Anxiety by Lowering Levels of Brain Amyloid Precursor Protein and Indoleamine 2,3-Dioxygenase in a Rat Model of Streptozotocin-Induced Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Umbelliprenin attenuates comorbid behavioral disorders in acetic acid-induced colitis in mice: mechanistic insights into hippocampal oxidative stress and neuroinflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Article
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- Minocycline Acts as a Neuroprotective Agent Against Tramadol-Induced Neurodegeneration: Behavioral and Molecular Evidence.International journal of preventive medicine · 2024Article
- Clinical and preclinical evaluation of miR-144-5p as a key target for major depressive disorder.CNS neuroscience & therapeutics · 2023Article
- Ellagic acid through attenuation of neuro-inflammatory response exerted antidepressant-like effects in socially isolated mice.Heliyon · 2023Article
- α7 Nicotinic acetylcholine receptor: a key receptor in the cholinergic anti-inflammatory pathway exerting an antidepressant effect.Journal of neuroinflammation · 2023Review
- Enhancing the Neuroprotection Potential of Edaravone in Transient Global Ischemia Treatment with Glutathione- (GSH-) Conjugated Poly(methacrylic acid) Nanogel as a Promising Carrier for Targeted Brain Drug Delivery.Oxidative medicine and cellular longevity · 2023Article
- Pexidartinib (PLX3397) through restoring hippocampal synaptic plasticity ameliorates social isolation-induced mood disorders.International immunopharmacology · 2022Article
- Challenges of repurposing tetracyclines for the treatment of Alzheimer's and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Neuroprotective Effect of Apigenin on Depressive-Like Behavior: Mechanistic Approach.Neurochemical research · 2022Article
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Neuroinflammation and mitochondrial dysfunction are suggested as mechanisms which are implicated in the pathophysiology of depression. Streptozotocin (STZ) is known to produce immune-inflammatory responses and mitochondrial dysfunction in different types of animal models of disease (e.g. type-1 diabetes and Alzheimer's disease). Therefore, a single low dose of Streptozotocin (STZ; intracerebroventricular, i.c.v, 0.2 mg/mouse) was used to induce an animal model of depression. The present study aims to investigate the effects of short (24 h) and long (14 days) exposure to minocycline on STZ-induced depressive-like behaviors (n = 6-8), hippocampal oxidative state biomarkers (n = 4), and the expression of hippocampal genes related to innate immunity (n = 3) in the hippocampus of male adult mice. In addition, the protective effects of different modes of minocycline (acute pretreatment (20 mg/kg, 1 h before STZ), acute post-treatment (20 mg/kg, 24 h after STZ), chronic pretreatment (5 mg/kg/day for 14 days before STZ), and chronic post-treatment (5 mg/kg/day for 14 days after STZ) were compared with the STZ effects. As the data showed, both short and long effects of STZ were associated with the depressive-like behaviors, abnormal mitochondrial function, and upregulation of neuroinflammatory genes in the hippocampus. Different modes of minocycline treatment could attenuate the negative impact of STZ on animals. The data suggested that minocycline at a human therapeutic dose (5 mg/kg) had protective effects against acute cellular damage induced by oxidation and the consequent inflammatory responses.
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