Protective effects of thymoquinone against acrylamide-induced liver, kidney and brain oxidative damage in rats

Abdel-Daim, Mohamed M.; El-Ela, Fatma I. Abo; Alshahrani, Fatima K.; Bin-Jumah, May; Al-Zharani, Mohammed; Almutairi, Bader O.; Alyousif, Mohamed S; Bungău, Simona; Aleya, Lotfi; Alkahtani, Saad

doi:10.1007/s11356-020-09516-3

Cited by 77 publications

(39 citation statements)

References 51 publications

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“…The first investigational evidence was provided in 2010, when a β-secretase inhibitor, GRL-8234, was employed to treat Tg2576 transgenic mice, and resulted in improved cognitive effects [ 54 ]. Moreover, soluble Aβ levels were also found to be retarded in mice [ 55 , 56 ] following GRL-8234 administration [ 54 ]. A significant reduction in Aβ plaque load was also observed in aged mice treated with GRL-8234 [ 57 ].…”

Section: Therapeutic Agents Targeting Amyloid Cascade Eventsmentioning

confidence: 99%

Exploring the Potential of Therapeutic Agents Targeted towards Mitigating the Events Associated with Amyloid-β Cascade in Alzheimer’s Disease

Behl

Kaur

Frățilă

et al. 2020

IJMS

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One of the most commonly occurring neurodegenerative disorders, Alzheimer’s disease (AD), encompasses the loss of cognitive and memory potential, impaired learning, dementia and behavioral defects, and has been prevalent since the 1900s. The accelerating occurrence of AD is expected to reach 65.7 million by 2030. The disease results in neural atrophy and disrupted inter-neuronal connections. Amongst multiple AD pathogenesis hypotheses, the amyloid beta (Aβ) cascade is the most relevant and accepted form of the hypothesis, which suggests that Aβ monomers are formed as a result of the cleavage of amyloid precursor protein (APP), followed by the conversion of these monomers to toxic oligomers, which in turn develop β-sheets, fibrils and plaques. The review targets the events in the amyloid hypothesis and elaborates suitable therapeutic agents that function by hindering the steps of plaque formation and lowering Aβ levels in the brain. The authors discuss treatment possibilities, including the inhibition of β- and γ-secretase-mediated enzymatic cleavage of APP, the immune response generating active immunotherapy and passive immunotherapeutic approaches targeting monoclonal antibodies towards Aβ aggregates, the removal of amyloid aggregates by the activation of enzymatic pathways or the regulation of Aβ circulation, glucagon-like peptide-1 (GLP-1)-mediated curbed accumulation and the neurotoxic potential of Aβ aggregates, bapineuzumab-mediated vascular permeability alterations, statin-mediated Aβ peptide degradation, the potential role of ibuprofen and the significance of natural drugs and dyes in hindering the amyloid cascade events. Thus, the authors aim to highlight the treatment perspective, targeting the amyloid hypothesis, while simultaneously emphasizing the need to conduct further investigations, in order to provide an opportunity to neurologists to develop novel and reliable treatment therapies for the retardation of AD progression.

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Section: Therapeutic Agents Targeting Amyloid Cascade Eventsmentioning

confidence: 99%

Exploring the Potential of Therapeutic Agents Targeted towards Mitigating the Events Associated with Amyloid-β Cascade in Alzheimer’s Disease

Behl

Kaur

Frățilă

et al. 2020

IJMS

Self Cite

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“…Plant products have potent protective effects against toxic insults [ [20] , [21] , [22] ]. However, several researchers have shown that many medicinal plants have potential toxicity on cellular and biochemical parameters of blood [ 23 , 24 ] and histopathology of various internal organs like the liver and kidney [ [25] , [26] , [27] , [28] , [29] ].…”

Section: Introductionmentioning

confidence: 99%

Sub-chronic toxicity of ethanol leaf extract of Syzygium guineense on the biochemical parameters and histopathology of liver and kidney in the rats

et al. 2021

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“…4 Recent studies showed that acrylamide caused oxidative brain damage by increasing Malondialdehyde (MDA) production in the brain tissue and reducing endogenous glutathione (GSH) concentrations as well as activities of antioxidant enzymes. [5][6][7][8] Moreover, it has been demonstrated that acrylamide produced neurotoxic effects by increasing the production of both oxidants and proinflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). [6][7][8][9] These literature data suggest that antioxidant and anti-inflammatory drugs can be useful in the treatment of the neurotoxicity of acrylamide.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Taxifolin on Acrylamide-induced Oxidative and Proinflammatory Brain Injury in Rats: A Biochemical and Histopathological Study

Ersoy¹,

Yaşar²,

Tanoğlu³

et al. 2021

IJPER

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Protective effects of thymoquinone against acrylamide-induced liver, kidney and brain oxidative damage in rats

Cited by 77 publications

References 51 publications

Exploring the Potential of Therapeutic Agents Targeted towards Mitigating the Events Associated with Amyloid-β Cascade in Alzheimer’s Disease

Exploring the Potential of Therapeutic Agents Targeted towards Mitigating the Events Associated with Amyloid-β Cascade in Alzheimer’s Disease

Sub-chronic toxicity of ethanol leaf extract of Syzygium guineense on the biochemical parameters and histopathology of liver and kidney in the rats

The Effect of Taxifolin on Acrylamide-induced Oxidative and Proinflammatory Brain Injury in Rats: A Biochemical and Histopathological Study

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