The effect of 3-nitropropionic acid on behavioral dysfunction, neuron loss and gliosis in the brain of adult male rats: The case of prefrontal cortex, hippocampus and the cerebellum

Torabi, Abolfazl; Joneidi, Mohammadjavad; Mohammadzadeh, Ibrahim; Abdollahifar, Mohammad‐Amin; Khatmi, Aysan; Ezi, Samira; Moghaddam, Meysam Hassani; Rafiei, Romina; Kahrizirad, Farshad; Norozian, Mohsen; Aliaghaei, Abbas

doi:10.1016/j.toxicon.2020.05.012

Cited by 13 publications

(1 citation statement)

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“…Rotarod, beam walking, and spontaneous locomotor activity tests were conducted on the animals, which revealed decreased grip strength, motor incoordination and imbalance, decreased motor activity, and increased immobility [ 1 , 2 , 3 , 8 ]. In addition, 3-NPA reduced the rat’s discrimination index during an object recognition test, indicating a significant decrease in cognitive performance [ 39 , 40 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations

Alharbi

2024

Biomedicines

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Huntington’s disease (HD) is a neurodegenerative disease that causes progressive motor and cognitive dysfunction. There is no cure for HD, and current therapeutics can only manage the signs and symptoms as well as slowing disease progression. This investigation examines the possible therapeutic advantages of europinidin in 3-nitropropionic acid (3-NPA) injected HD in rats. Wistar rats were randomly assigned to five groups (n = 6): normal control, 3-NPA (10 mg/kg, i.p.), 3-NPA + europinidin-10 (10 mg/kg, p.o.), 3-NPA + europinidin-20 (20 mg/kg, p.o.), and europinidin alone (20 mg/kg, p.o.) for 15-day. Various behavioral and biochemical parameters including antioxidant levels, oxidative stress, pro-inflammatory markers, mitochondrial enzyme complex, and neurotransmitters were assessed. Europinidin restored biochemical, mitochondrial dysfunction, oxidative stress, neurotransmitter, and pro-inflammatory parameters disrupted by 3-NPA. Here we show that europinidin attenuates 3-NPA-induced neurodegeneration in rat models of HD. Europinidin modulates oxidative stress, enhances antioxidants, restores mitochondrial enzyme complex activity, reduces neuroinflammation, and modulates neurotransmitter levels. Our findings reveal the potential of europinidin as a novel therapeutic agent for the treatment of HD. This study also provides new insights into the molecular mechanisms of europinidin-mediated neuroprotection and may have a beneficial role in the management of neurological diseases.

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