Effects of carvacrol and physical exercise on motor and memory impairments associated with Parkinson’s disease

Hamzehloei, Leila; Rezvani, Mohammad Ebrahim; Rajaei, Ziba

doi:10.1590/0004-282x20190079

Cited by 11 publications

(6 citation statements)

References 35 publications

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“…Furthermore, the role of oxidative stress in the acrylamide induced toxicity is proved in other studies (35)(36)(37). However, carvacrol could increase the level of GSH in cells treated with acrylamide or H 2 O 2 , which is in compliance with other experimental studies (37)(38)(39). Consequently, in this study, reduced lipid peroxidation and increased glutathione concentration, induced by carvacrol, may have an important role in the protection against senescent in fibroblast cells.…”

Section: Discussionsupporting

confidence: 89%

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Acrylamide Induced Oxidative Cellular Senescence in Embryonic Fibroblast Cell Line (NIH 3T3): A Protection by Carvacrol

Evazalipour

Kozani

et al. 2021

Jundishapur J Nat Pharm Prod

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Background: Stress-induced cellular senescence is a perpetual state of cell cycle arrest occurring in proliferating cells in response to stressful conditions. It is believed that oxidative stress plays a unique role in this process. As a reactive chemical compound that can induce oxidative stress, acrylamide is widely applied in several fields. Carvacrol is a liquid phenolic monoterpenoid found in essential oils of some plants and is known for its antioxidant and anticarcinogenic properties. Objectives: The current study aimed to evaluate the effects of carvacrol on oxidative stress and cellular senescence induced by acrylamide in the NIH 3T3 cell line. Methods: NIH 3T3 embryonic fibroblast cells were exposed to different concentrations of acrylamide, carvacrol, and H2O2 in a cell culture medium. The level of β-galactosidase (SA-β-gal) activity, as a marker of cellular senescence, was measured using staining and quantitative assays. Furthermore, to measure oxidative stress parameters, the content of glutathione and lipid peroxidation were determined. Results: Acrylamide could induce premature senescence evident by the elevated lipid peroxidation and SA-β-gal activity and declined cell viability and glutathione. Moreover, carvacrol showed beneficial effects on both acrylamide- and H2O2-induced cellular senescence by significantly reversing or subsiding the effect of oxidative stress and mediating its consequences. Conclusions: It can be concluded that carvacrol has protective effects against oxidative cellular senescence induced by acrylamide in the NIH 3T3 cell line.

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Section: Discussionsupporting

confidence: 89%

“…Furthermore, carvacrol treatment effectively reduced the level of lipid peroxidation in the acrylamide-and H 2 O 2 -treated cell groups. Earlier studies point that carvacrol inhibits lipid peroxidation by direct scavenging and inhibition of ROS production (37)(38)(39).…”

Section: Discussionmentioning

confidence: 99%

Acrylamide Induced Oxidative Cellular Senescence in Embryonic Fibroblast Cell Line (NIH 3T3): A Protection by Carvacrol

Evazalipour

Kozani

et al. 2021

Jundishapur J Nat Pharm Prod

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“…Neuroplasticity is improved by changing the synaptic structure and function in different regions of brain and also modulates multiple systems that regulate glial activation and neuro-inflammation [ 52 ]. Furthermore, exercising, in addition to carvacrol (a food additive), is also helpful in reducing rotational behavior and improves aversive memory deficit and decreases lipid peroxidation levels, along with increasing total thiol concentration in the hippocampus and/or hemi-Parkinson rats [ 53 ]. This indicates that this combination of carvacrol and treadmill exercise can be an effective therapeutic tool to treat neuro-behavioral deficits in PD patients [ 53 ].…”

Section: Physical Exercise and Neurodegenerative Diseasementioning

confidence: 99%

“…Furthermore, exercising, in addition to carvacrol (a food additive), is also helpful in reducing rotational behavior and improves aversive memory deficit and decreases lipid peroxidation levels, along with increasing total thiol concentration in the hippocampus and/or hemi-Parkinson rats [ 53 ]. This indicates that this combination of carvacrol and treadmill exercise can be an effective therapeutic tool to treat neuro-behavioral deficits in PD patients [ 53 ]. Regular exercise also contributes to health in PD patients as it improves the ability of the patient to adapt to barriers encountered during gait, regardless of the medication state [ 54 ].…”

Section: Physical Exercise and Neurodegenerative Diseasementioning

confidence: 99%

Possible Neuroprotective Mechanisms of Physical Exercise in Neurodegeneration

Mahalakshmi

Maurya²,

Lee

et al. 2020

IJMS

140

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Physical exercise (PE) improves physical performance, mental status, general health, and well-being. It does so by affecting many mechanisms at the cellular and molecular level. PE is beneficial for people suffering from neuro-degenerative diseases because it improves the production of neurotrophic factors, neurotransmitters, and hormones. PE promotes neuronal survival and neuroplasticity and also optimizes neuroendocrine and physiological responses to psychosocial and physical stress. PE sensitizes the parasympathetic nervous system (PNS), Autonomic Nervous System (ANS) and central nervous system (CNS) by promoting many processes such as synaptic plasticity, neurogenesis, angiogenesis, and autophagy. Overall, it carries out many protective and preventive activities such as improvements in memory, cognition, sleep and mood; growth of new blood vessels in nervous system; and the reduction of stress, anxiety, neuro-inflammation, and insulin resistance. In the present work, the protective effects of PE were overviewed. Suitable examples from the current research work in this context are also given in the article.

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“…(emulsified with 1% Tween 80 and dissolved in normal saline) throughout the investigation. [42][43][44] • Group 4 (AA+CRV): Standard rat chow was given ad-libitum during the experiment. A total of 40 mg/kg AA (Sigma) dissolved in drinking water was administrated by gavage and 50 mg/kg CRV was administrated i.p.…”

Section: Animals and Experimental Protocolmentioning

confidence: 99%

Metabolomic modelling and neuroprotective effects of carvacrol against acrylamide toxicity in rat's brain and sciatic nerve

Durmus,

Burak,

Goktug

et al. 2024

Clin Exp Pharma Physio

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The study aimed to investigate the harmful effects of acrylamide (AA), which forms in carbohydrate‐rich foods at temperatures above 120°C, on the central and peripheral nervous systems and to evaluate the potential neuroprotective effects of carvacrol (CRV). Male Wistar Albino rats were subjected to AA (40 mg/kg/bw/day) and CRV (50 mg/kg/bw/day) for 15 days. Following the last administration, evaluations revealed disrupted gait, heightened thermal sensitivity and altered paw withdrawal thresholds in AA‐exposed rats. Notably, AA reduced glutathione (GSH) and raised malondialdehyde (MDA) levels in both brain and sciatic nerve tissues. AA raised nuclear factor erythroid 2‐related factor 2 (Nrf2), caspase 3 and nuclear factor κB (NF‐κB) gene expressions while decreasing NR4A2. CRV co‐administration mitigated gait abnormalities, elevated GSH levels and lowered MDA levels in both tissues. CRV also modulated gene expression, reducing Nrf2 and NF‐κB while increasing NR4A2. Histopathological signs of AA‐induced neurodegeneration and elevated glial fibrillary acidic protein levels observed in brain and sciatic nerve tissues were rectified with simultaneous administration of CRV, thereby demonstrating neuroprotective efficacy in both regions. This study is pioneering in demonstrating CRV's neuroprotective potential against AA‐induced neurotoxicity in both central and peripheral nervous systems, effectively addressing limitations in the literature. In conclusion, the study revealed AA‐induced neurodegeneration in the brain and sciatic nerve, with CRV significantly mitigating this neurotoxicity. This novel research underscores CRV's promise as a neuroprotective agent against AA‐induced adverse effects in both the central and peripheral nervous systems.

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Effects of carvacrol and physical exercise on motor and memory impairments associated with Parkinson’s disease

Cited by 11 publications

References 35 publications

Acrylamide Induced Oxidative Cellular Senescence in Embryonic Fibroblast Cell Line (NIH 3T3): A Protection by Carvacrol

Acrylamide Induced Oxidative Cellular Senescence in Embryonic Fibroblast Cell Line (NIH 3T3): A Protection by Carvacrol

Possible Neuroprotective Mechanisms of Physical Exercise in Neurodegeneration

Metabolomic modelling and neuroprotective effects of carvacrol against acrylamide toxicity in rat's brain and sciatic nerve

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