ArticleIranian journal of basic medical sciences2020
Bee venom attenuates neurodegeneration and motor impairment and modulates the response to L-dopa or rasagiline in a mice model of Parkinson's disease.
Article in Iranian journal of basic medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Brain-targeted intranasal aripiprazole via modified chitosan nanoparticles: controlled release, pharmacokinetics, and pharmacodynamics.Drug delivery and translational research · 2026Article
- Bee venom enhances dopaminergic function and behavioral recovery in a murine model of Parkinson's disease.Neuroprotection (Chichester, England) · 2026Article
- Bee venom acupuncture therapy ameliorates ulcerative colitis by reducing inflammatory response, oxidative stress, and suppressing the NF-κB/HIF-1α pathway.Open life sciences · 2026Article
- Therapeutic Bioactivity Exerted by theMolecules (Basel, Switzerland) · 2025Article
- Article
- Chemical composition and studying the possible neuroprotective effect of iridoids-rich fraction from Pentas lanceolata leaves using rotenone model of Parkinson's disease in mice.Inflammopharmacology · 2024Article
- Beneficial Effect of Bee Venom and Its Major Components on Facial Nerve Injury Induced in Mice.Biomolecules · 2023Article
- Wasp venom fromPharmaceutical biology · 2022Article
- Pharmacological effects and mechanisms of bee venom and its main components: Recent progress and perspective.Frontiers in pharmacology · 2022Review
- Effect of Acupuncture on Movement Function in Patients with Parkinson's Disease: Network Meta-Analysis of Randomized Controlled Trials.Healthcare (Basel, Switzerland) · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
objectivesThis study aimed to investigate the effect of bee venom, a form of alternative therapy, on rotenone-induced Parkinson's disease (PD) in mice. Moreover, the possible modulation by bee venom of the effect of L-dopa/carbidopa or rasagiline was examined. MATERIALS AND
methodsRotenone (1.5 mg/kg, subcutaneously; SC) was administered every other day for two weeks and at the same time mice received the vehicle (DMSO, SC), bee venom (0.065, 0.13, and 0.26 mg/kg; intradermal; ID), L-dopa/carbidopa (25 mg/kg, intraperitoneal; IP), L-dopa/carbidopa+bee venom (0.13 mg/kg, ID), rasagiline (1 mg/kg, IP) or rasagiline+bee venom (0.13 mg/kg, ID). Then, wire hanging and staircase tests were performed and mice were euthanized and brains' striata separated. Oxidative stress biomarkers namely, malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), paraoxonase-1 (PON-1), and total antioxidant capacity (TAC) were measured. Additionally, butyrylcholinesterase (BuChE), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), and dopamine (DA) were evaluated. Brain histopathological changes and caspase-3- expression were done.
resultsBee venom significantly enhanced motor performance and inhibited rotenone-induced oxidative/nitrosative stress, observed as a reduction in both MDA and NO along with increasing GSH, PON-1, and TAC. Besides, bee venom decreased MCP-1, TNF-α, and caspase-3 expression together with an increase in BuChE activity and DA content.
conclusionBee venom alone or in combination with L-dopa/carbidopa or rasagiline alleviated neuronal degeneration compared with L-dopa/carbidopa or rasagiline treatment only. Bee venom via its antioxidant and cytokine reducing potentials might be of value either alone or as adjunctive therapy in the management of PD.
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