Neuroprotective Efficacy of Eugenol and Isoeugenol in Acrylamide-Induced Neuropathy in rats: Behavioral and Biochemical evidence

Prasad, Sathya N; Muralidhara, .

doi:10.1007/s11064-012-0924-9

Cited by 104 publications

(58 citation statements)

References 62 publications

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“…The ability of eugenol to directly suppress the enhanced AChE activity following Al intoxication in the current study could be explained with the finding of an in vitro study that demonstrated a potential anti-cholinesterase property of eugenol (51). Similarly, eugenol was found to normalise the cortical AChE level in acrylamide-induced brain neuropathy in rats (21).…”

Section: Figure 3 Effect Of Eugenol And/or Aluminium On Brain Acetylcsupporting

confidence: 60%

“…AChE is a significant biological component of the membrane that contributes to its integrity. Induction of the AChE activity causes faster acetylcholine degradation and consequent lowered stimulation of acetylcholine receptors, which produces a reduction of diverse cholinergic (learning and memory), as well as non-cholinergic (cell proliferation and neurite outgrowth) functions (12,21). In the current study, sub-chronic administration of Al induced significantly the brain AChE activity.…”

Section: Figure 3 Effect Of Eugenol And/or Aluminium On Brain Acetylcsupporting

confidence: 45%

“…Furthermore, it prevented from 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in mouse striatum (19) and provided a neuroprotective effect against hippocampal CA1 neuronal ischemia-induced injury in gerbils (20). It also proved to protect against acrylamide-induced neuropathy (21) and chlorpyrifos-induced brain toxicity (12) in rats, which may at least in part be attributed to its antioxidative stress activity.…”

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confidence: 99%

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Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

Said

Rabo

2017

Archives of Industrial Hygiene and Toxicology

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Aluminium (Al) is a neurotoxic metal that contributes to the progression of several neurodegenerative diseases. The aim of the present study was to evaluate the protective effect of dietary eugenol supplementation against aluminium (Al)- induced cerebral damage in rats. Male Wistar rats were divided into four groups: normal controls, rats fed a diet containing 6,000 μg g-1 eugenol, rats intoxicated daily with aluminium chloride (84 mg kg-1 body weight) p. o. and fed either a basal diet or a eugenol-containing diet. Daily oral administration of Al for four consecutive weeks to rats significantly reduced brain total antioxidant status (TAS) (11.42±0.31 μmol g-1 tissue, p<0.001) with a subsequent significant enhancement of lipid peroxidation (MDA) (32.55±1.68 nmol g-1 tissue, p<0.002). In addition, Al enhanced brain acetylcholinesterase activity (AChE) (46.22±4.90 U mg-1 protein, p<0.001), tumour necrosis factor alpha (TNF-α) (118.72±11.32 pg mg-1 protein, p<0.001), and caspase 3 (Casp-3) (8.77±1.26 ng mg-1 protein, p<0.001) levels, and in contrast significantly suppressed brain-derived neurotrophic factor (BDNF) (82.74±14.53 pg mg-1 protein, p<0.002) and serotonin (5-HT) (1.54±0.12 ng mg-1 tissue, p<0.01) levels. Furthermore, decreased glial fibrillary acidic protein (GFAP) immunostaining was noticed in the striatum of Al-intoxicated rats, compared with untreated controls. On the other hand, co-administration of dietary eugenol with Al intoxication restored brain BDNF (108.76±2.64 pg mg-1 protein) and 5-HT (2.13±0.27 ng mg-1 tissue) to normal levels, enhanced brain TAS (13.43±0.24 μmol g-1 tissue, p<0.05), with a concomitant significant reduction in TNF-α (69.98±4.74 pg mg-1 protein) and Casp-3 (3.80±0.37 ng mg-1 protein) levels (p<0.001), as well as AChE activity (24.50±3.25 U mg-1 protein, p<0.001), and increased striatal GFAP immunoreactivity, compared with Al-treated rats. Histological findings of brain tissues verified biochemical data. In conclusion, eugenol holds potential as a neuroprotective agent through its hydrophobic, antioxidant, and anti-apoptotic properties, as well as its neurotrophic ability against Al-induced brain toxicity in rats.

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Section: Figure 3 Effect Of Eugenol And/or Aluminium On Brain Acetylcsupporting

confidence: 60%

Section: Figure 3 Effect Of Eugenol And/or Aluminium On Brain Acetylcsupporting

confidence: 45%

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confidence: 99%

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Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

Said

Rabo

2017

Archives of Industrial Hygiene and Toxicology

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“…To test if other xenobiotics are capable of activating wdr-23, we also tested the neurotoxin and suspected carcinogen acrylamide, an electrophile present in cooked food (41) that forms protein adducts (42), elevates reactive oxygen species and lipid peroxidation, depletes glutathione (43,44), and strongly activates SKN-1 target genes in C. elegans (45). As shown in Fig.…”

Section: R E T R a C T E Dmentioning

confidence: 99%

A Negative-Feedback Loop between the Detoxification/Antioxidant Response Factor SKN-1 and Its Repressor WDR-23 Matches Organism Needs with Environmental Conditions

Leung

Wang

Deonarine

et al. 2013

Molecular and Cellular Biology

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Negative-feedback loops between transcription factors and repressors in responses to xenobiotics, oxidants, heat, hypoxia, DNA damage, and infection have been described. Although common, the function of feedback is largely unstudied. Here, we define a negative-feedback loop between the Caenorhabditis elegans detoxification/antioxidant response factor SKN-1/Nrf and its repressor wdr-23 and investigate its function in vivo. Although SKN-1 promotes stress resistance and longevity, we find that tight regulation by WDR-23 is essential for growth and reproduction. By disabling SKN-1 transactivation of wdr-23, we reveal that feedback is required to set the balance between growth/reproduction and stress resistance/longevity. We also find that feedback is required to set the sensitivity of a core SKN-1 target gene to an electrophile. Interestingly, the effect of feedback on target gene induction is greatly reduced when the stress response is strongly activated, presumably to ensure maximum activation of cytoprotective genes during potentially fatal conditions. Our work provides a framework for understanding the function of negative feedback in inducible stress responses and demonstrates that manipulation of feedback alone can shift the balance of competing animal processes toward cell protection, health, and longevity. P rotective responses to cellular stress are coordinated by inducible transcription factors. Tight regulation of stress responses is essential, because they may have consequences for important processes such as growth, development, and reproduction. Negative feedback is a fundamental strategy for regulation of homeostatic processes at all levels of physiology. Simple two-component negative-feedback loops in which a transcription factor induces the expression of an interacting protein that represses the transcription factor are found within responses to diverse stressors, including DNA damage (1), oxidants (2), hypoxia (3), heat shock (4), and infection (5). Although the general importance of repression is recognized, the regulatory and physiological importance of feedback is unexplored.The Cap 'n' Collar (CNC) family of transcription factors orchestrates inducible antioxidant and detoxification responses in animal cells (6). CNC factors activate the expression of genes encoding enzymes that scavenge free radicals, synthesize glutathione, detoxify and export xenobiotics, and repair damage to proteins (6, 7). CNCs promote longevity in invertebrate models (8-11), and increased CNC activity is associated with long-lived and stress-resistant strains of mice (12). The main inducible CNC in humans is Nrf2, which is a popular chemopreventative target for diverse pathologies, including cancer, neurodegeneration, inflammation, asthma, and aging (13-16).Nrf2 is an unstable protein that is targeted for degradation by KEAP1, a Kelch repeat protein that functions as an adaptor for the CUL3 ubiquitin ligase. Oxidative modification of KEAP1 releases Nrf2 and allows it to accumulate and activate a cytoprotective gene expre...

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“…Exposure to ACR elevates the generation of reactive oxygen species and induces apoptosis in PC12 cells (9). Also, in rodent models, it has caused lipid peroxidation, depletion in GSH levels, and alterations in apoptotic markers (8,(10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the Neuroprotective Effect of Silymarin on Acrylamide-Induced Neurotoxicity

Mehri

Dadesh

Tabeshpour

et al. 2016

Jundishapur J Nat Pharm Prod

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Neuroprotective Efficacy of Eugenol and Isoeugenol in Acrylamide-Induced Neuropathy in rats: Behavioral and Biochemical evidence

Cited by 104 publications

References 62 publications

Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

A Negative-Feedback Loop between the Detoxification/Antioxidant Response Factor SKN-1 and Its Repressor WDR-23 Matches Organism Needs with Environmental Conditions

Evaluation of the Neuroprotective Effect of Silymarin on Acrylamide-Induced Neurotoxicity

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