Nano-ivabradine averts behavioral anomalies in Huntington's disease rat model via modulating Rhes/m-tor pathway

Saad, Marina; Ahmed, Maha A.E.; Elbadawy, Norhan N.; Abdelkader, Noha F.

doi:10.1016/j.pnpbp.2021.110368

Cited by 9 publications

(3 citation statements)

References 73 publications

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“…Europinidin might influence neurotransmitter levels by inhibiting AChE activity, increasing GABA levels, and promoting DA synthesis or release. These actions could help restore neurotransmitter balance, which is often disrupted in HD [ 45 , 46 , 47 , 48 , 49 , 50 ].…”

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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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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“…Degeneration of MSN neurons could be seen in the striatum and cortex of HD patients. In HD-induced rats’ brains, H- and E-staining revealed morphological abnormalities, apoptotic cells, cells losing nucleus and membrane, degenerative neurons, and gliosis [ 96 ]. The neurotoxin 3-NP caused neurodegeneration and was found in HD patients [ 97 , 98 ].…”

Section: Discussionmentioning

confidence: 99%

Beta-Boswellic Acid Reverses 3-Nitropropionic Acid-Induced Molecular, Mitochondrial, and Histopathological Defects in Experimental Rat Model of Huntington’s Disease

Albekairi

Kamra²,

Bhardwaj³

et al. 2022

Biomedicines

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Huntington’s disease (HD) is distinguished by a triple repeat of CAG in exon 1, an increase in poly Q in the Htt gene, and a loss of GABAergic medium spiny neurons (MSN) in the striatum and white matter of the cortex. Mitochondrial ETC-complex dysfunctions are involved in the pathogenesis of HD, including neuronal energy loss, synaptic neurotrophic decline, neuronal inflammation, apoptosis, and grey and white matter destruction. A previous study has demonstrated that beta Boswellic acid (β-BA), a naturally occurring phytochemical, has several neuroprotective properties that can reduce pathogenic factors associated with various neurological disorders. The current investigation aimed to investigate the neuroprotective potential of β-BA at oral doses of 5, 10, and 15 mg/kg alone, as well as in conjunction with the potent antioxidant vitamin E (8 mg/kg, orally) in 3-NP-induced experimental HD rats. Adult Wistar rats were separated into seven groups, and 3-NP, at a dose of 10 mg/kg, was orally administered to each group of adult Wistar rats beginning on day 1 and continuing through day 14. The neurotoxin 3-NP induces neurodegenerative, g, neurochemical, and pathological alterations in experimental animals. Continuous injection of 3-NP, according to our results, aggravated HD symptoms by suppressing ETC-complex-II, succinate dehydrogenase activity, and neurochemical alterations. β-BA, when taken with vitamin E, improved behavioural dysfunctions such as neuromuscular and motor impairments, as well as memory and cognitive abnormalities. Pharmacological treatments with β-BA improved and restored ETC complexes enzymes I, II, and V levels in brain homogenates. β-BA treatment also restored neurotransmitter levels in the brain while lowering inflammatory cytokines and oxidative stress biomarkers. β-BA’s neuroprotective potential in reducing neuronal death was supported by histopathological findings in the striatum and cortex. As a result, the findings of this research contributed to a better understanding of the potential role of natural phytochemicals β-BA in preventing neurological illnesses such as HD.

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“…The results demonstrated that the nano formulation treatment significantly ameliorated behavioral performance and mitigated the oxidative stress in a rats model induced by 3‐nitropropionic acid, which presented as a potent therapeutic option for the effective treatment of HD. Additionally, thymoquinone (Ramachandran & Thangarajan, 2018), epigallocatechin‐3‐gallate (EGCG; Cano et al, 2021), cholesterol (Birolini et al, 2021; Valenza et al, 2015) and ivabradine (Saad et al, 2021) were developed as nanoparticles for the treatment of HD (Table 3).…”

Section: Nanotechnology‐empowered Therapeutics In Hdmentioning

confidence: 99%

Nanotechnology‐empowered therapeutics targeting neurodegenerative diseases

Wang

Gonzalez

Cordova

et al. 2023

WIREs Nanomed Nanobiotechnol

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Neurodegenerative diseases are posing pressing health issues due to the high prevalence among aging populations in the 21st century. They are evidenced by the progressive loss of neuronal function, often associated with neuronal necrosis and many related devastating complications. Nevertheless, effective therapeutical strategies to treat neurodegenerative diseases remain a tremendous challenge due to the multisystemic nature and limited drug delivery to the central nervous system. As a result, there is a pressing need to develop effective alternative therapeutics to manage the progression of neurodegenerative diseases. By utilizing the functional reconstructive materials and technologies with specific targeting ability at the nanoscale level, nanotechnology‐empowered medicines can transform the therapeutic paradigms of neurodegenerative diseases with minimal systemic side effects. This review outlines the current applications and progresses of the nanotechnology‐enabled drug delivery systems to enhance the therapeutic efficacy in treating neurodegenerative diseases.This article is categorized under: Therapeutic Approaches and Drug Discovery > Nanomedicine for Neurological Disease Therapeutic Approaches and Drug Discovery > Emerging Technologies

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Nano-ivabradine averts behavioral anomalies in Huntington's disease rat model via modulating Rhes/m-tor pathway

Cited by 9 publications

References 73 publications

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

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

Beta-Boswellic Acid Reverses 3-Nitropropionic Acid-Induced Molecular, Mitochondrial, and Histopathological Defects in Experimental Rat Model of Huntington’s Disease

Nanotechnology‐empowered therapeutics targeting neurodegenerative diseases

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