ArticleInflammopharmacology2024
Empagliflozin repurposing in Parkinson's disease; modulation of oxidative stress, neuroinflammation, AMPK/SIRT-1/PGC-1α, and wnt/β-catenin pathways.
Article in Inflammopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Neuroinflammation and noradrenergic modulation with β2-adrenoceptors: Emerging therapeutic targets for Parkinson's diseases.Neural regeneration research · 2026Article
- Neuroprotective effects of empagliflozin and metformin combined therapy on rotenone induced Parkinsonism in Wistar rats via PI3K and PPARγ modulation.Scientific reports · 2026Article
- Canagliflozin attenuates Parkinson's disease and is associated with modulation of gut-inflammasome-brain axis in rats.Inflammopharmacology · 2026Article
- Internal Heat Acupuncture Treatment Inhibits Ferroptosis in the Spinal Dorsal Horn in Neurotoxin-Induced Parkinson's Disease Rats.Applied biochemistry and biotechnology · 2026Article
- Identification of novel small molecules as potential SGLT2 inhibitors through combined virtual screening and experimental validation.Molecular diversity · 2026Article
- Dapagliflozin ameliorates motor deficits in a Parkinson's disease model induced by 6-OHDA: An integrative in vivo and in silico approach from α-synuclein/A2AAR/TH/TNF-α to APAF-1/caspase-3 modulation.Inflammopharmacology · 2026Article
- Repurposing Antidiabetic Medications for Parkinson's Disease: Focus on Biomarker Strategies for Disease Modification.International journal of molecular sciences · 2026Review
- From Glucose Transport to Microbial Modulation: The Impact of Sodium Glucose Co-Transporter-2 Inhibitors on the Gut Microbiota.Medical sciences (Basel, Switzerland) · 2026Review
- Neurodegeneration at the crossroads: the gut-brain axis and blood-brain barrier in Parkinson's disease - a review.Frontiers in pharmacology · 2026Review
- Chemical composition ofFrontiers in pharmacology · 2026Article
- Sodium-Glucose Cotransporter-2 Inhibitors in Mood Disorders: A Narrative Review of Mechanisms, Evidence, and Challenges.Neuropsychiatric disease and treatment · 2026Review
- Beyond the Cardio-Renal-Metabolic Axis: Emerging Therapeutic Targets and Novel Mechanisms of Action of Flozins.Journal of clinical medicine · 2025Review
- Empagliflozin Protects Against Oxidative Stress in the Diabetic Brain by Inducing HPharmaceuticals (Basel, Switzerland) · 2025Article
- Parkinson's Disease: Bridging Gaps, Building Biomarkers, and Reimagining Clinical Translation.Cells · 2025Review
- The SGLT2 Inhibitor Empagliflozin Mitigates the Harmful Effects of Methylglyoxal Exposure on Ovalbumin-Induced Mouse Airway Inflammation.International journal of molecular sciences · 2025Article
- Empagliflozin and memantine combination ameliorates cognitive impairment in scopolamine + heavy metal mixture-induced Alzheimer's disease in rats: role of AMPK/mTOR, BDNF, BACE-1, neuroinflammation, and oxidative stress.Inflammopharmacology · 2025Article
- Intranasal delivery of blackberry-loaded Chitosan nanoparticles for antipsychotic potential in Ketamine-induced schizophrenia in rats.Scientific reports · 2025Article
- Developmental and Neuroprotective Effects of α-Terpineol in MPTP-Induced Parkinsonism in Zebrafish Larvae.Neurochemical research · 2025Article
- Article
- Unlocking Hope: Therapeutic Advances and Approaches in Modulating the Wnt Pathway for Neurodegenerative Diseases.Molecular neurobiology · 2025Review
Corrections and comments
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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
Parkinson's disease is a neuroprogressive disorder characterized by loss of dopaminergic neurons in substantia nigra pars compacta. Empagliflozin (EMPA), a SGLT-2 inhibitor, is an oral hypoglycemic agent with reported anti-inflammatory and antioxidant effects. The current study aimed to evaluate the neuroprotective effect of EMPA in rotenone-induced Parkinson's disease. Rats were randomly distributed among five groups as follows: control, rotenone (2 mg/kg), rotenone + EMPA (10 mg/kg), rotenone + EMPA (20 mg/kg), and EMPA (20 mg/kg) groups. They were treated for 30 consecutive days. Rotenone reduced locomotor activity and retention time on the rotarod performance test while elongated descent latency time. On the other side, EMPA corrected these behavioral changes. These results were confirmed by histological examination and number of intact neurons. Moreover, rotenone induced alpha-synuclein accumulation, reduced tyrosine hydroxylase expression, dopamine, 3,4-dihydroxyphenylacetic acid, and homovanillic acid concentrations. On the other side, EMPA reversed such effects induced by rotenone. Depending on previous results, EMPA (20 mg/kg) was selected for further mechanistic studies. Rotenone ameliorated superoxide dismutase and catalase activities and enhanced lipid peroxidation, interleukin-1β, and tumor necrosis factor-α levels. By contrast, EMPA opposed rotenone-induced effects on oxidative stress and inflammation. Besides, rotenone reduced the expression of pAMP-activated protein kinase (pAMPK), peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α), and Sirtuin-1 (SIRT-1), as well as abrogated NAD
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