Evaluation of Glucosamine Effect Against Heart and Brain Damage Induced by Y-radiation or Aluminium Chloride in Female Rats

Hawas, Asrar M.; Rashed, Laila Ahmed; Mohamed, Marwa Abd El Hameed

doi:10.1590/1678-4324-2020180687

Cited by 4 publications

(8 citation statements)

References 63 publications

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“…66 As well, glucosamine could be used to improve heart and brain damage induced by gamma radiation exposure or aluminum chloride due to its antioxidant effect. 4…”

Section: Discussionmentioning

confidence: 99%

“…Forty rats were randomly classified into four groups (n = 10/group) as follows: Group 1 (control): rats were administered distilled water. Group 2 (irradiation): rats were administered vehicle alone (distilled water) and exposed to fractionated doses of whole-body gamma radiation at a dose level of 8 Gy 4 (2 Gy for 4 consecutive days). Group 3 (glucosamine): rats treated with 1 g/kg glucosamine, P.O.…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, it is considered an effective therapeutic agent for treating osteoarthritis, 14 gastritis, and inflammatory bowel diseases, 15 as well as lung injury. 16 Glucosamine is found to be a major constituent of brain glycogen, in addition, it has a protective effect against brain damage, 4,17 but its role in managing depression-like effect has not been established yet. Glucosamine is considered an effective compound in the health care field as it could alleviate oxidative stress through its multiple antioxidant activities as glucosamine showed a significant reducing power and superoxide/hydroxyl-radical scavenging ability.…”

Section: Introductionmentioning

confidence: 99%

“…2,3 Exposure to whole-body gamma radiation (8 Gy) significantly caused neural disorders. 4 Recently, it has been found that brain irradiation (8 Gy, 2 fractions) induced microvascular cognitive impairment in juvenile murine unilateral hippocampal synaptic plasticity. 5 The brain is affected by radiation exposure according to age, brain region, and sex.…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of Glycogen Synthase Kinase Pathway for Assessing the Antidepressant-like Effect of Glucosamine as a Radioprotector in Rats: Behavioral and Biochemical Studies

Mekkawy,

Karam,

Mohamed

et al. 2023

Dose-Response

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Radiotherapy is a very important tool in the treatment of cancer; nevertheless, its side effects are a hindrance to its use. The present study is designed to evaluate glucosamine effects against radiation-induced brain oxidative stress and depression-like effect in rats. Four groups of female Wister rats were used as control, irradiated (4 × 2 Gy), glucosamine (1 g/kg P.O), and glucosamine + irradiated group. The behavioral responses are estimated. The brain hippocampi of the rats are separated to evaluate oxidative stress biochemical parameters and glycogen synthase kinase pathway in addition to the biogenic amines. Irradiation exposure led to disturbances in the behavioral assessments (forced swimming test, light–dark box, and open field test) and a significant decrease in brain GSH, neurotransmitters (serotonin, norepinephrine, and dopamine), phosphatidylinositol 3 kinase (PI3K), and phosphorylated protein kinase-B (p-AKT) levels. Additionally, MDA and ROS levels increased significantly post-irradiation along with the phosphorylated glycogen synthase kinase (p-GSK3). Glucosamine administration before irradiation caused improvement in the behavioral valuations and the biochemical parameters in the brain as well. Glucosamine might be used as a radioprotector to improve brain function and as an antidepressant drug. It could be promising as a future therapy in managing depression occurring during radiotherapy.

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“…66 As well, glucosamine could be used to improve heart and brain damage induced by gamma radiation exposure or aluminum chloride due to its antioxidant effect. 4…”

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Evaluation of Glycogen Synthase Kinase Pathway for Assessing the Antidepressant-like Effect of Glucosamine as a Radioprotector in Rats: Behavioral and Biochemical Studies

Mekkawy,

Karam,

Mohamed

et al. 2023

Dose-Response

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“…Similarly, among such other chemical compounds, aluminium chloride (AlCl 3 ) and sodium azide (NaN 3 ) have been specifically experimented for the induction of neurological and other disease symptoms. , AlCl 3 has been known to have a tendency to accumulate in various tissues of the body such as liver, pancreas, kidney, brain, and heart. It has been associated with hepatic dysfunction, nephron toxicity, neurotoxicity, and cardiotoxicity ,, via generation of ROS species and induction of oxidative stress, mitochondrial dysfunction, and lipid peroxidation. Further, the molecular basis for the effect of AlCl 3 toxicity may include the reduction in neuronal plasticity and suppressed axon maintenance in the hippocampus .…”

Section: Introductionmentioning

confidence: 99%

Comparative Biochemical Profiling of Aluminum Chloride and Sodium Azide Induced Neuroinflammation and Cardiometabolic Disturbance

et al. 2022

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Comorbidities in human beings signify the numerous risk factors that increase the incidences of neuro- and cardio-metabolic disorders. Experimental models depicting comorbidities are important to explore the molecular pathophysiology that can help suggest appropriate treatment strategies. Tissue-accumulating potential and pathological effects of aluminium chloride (AlCl3)and sodium azide (NaN3) are well recognized. Hence, in the current work, we have for the first time aimed to investigate the unexplored potential of graded dose effects of AlCl3 and NaN3 in inducing early inflammation and cardiometabolic toxicity via comparative biochemical analysis of AlCl3 and/or NaN3. Rats were allocated into seven groups (n = 6). Group 1 was normal control. Remaining groups were given graded doses of AlCl3 and/or NaN3, as LD-AlCl3 (AlCl3 40 mg), MD-AlCl3 (AlCl3 45 mg), and HD-AlCl3 (AlCl3 50 mg) representing low dose, medium dose, and high dose of AlCl3, respectively, and the remaining as LD-NaN3 (NaN3 13 mg), MD-NaN3 (NaN3 15 mg), and HD-NaN3 (NaN3 17 mg) representing low dose, medium dose, and high dose of NaN3, respectively. Serum levels of glucose, insulin, lipid profile, inflammatory mediators like IL-6 and oxidative stress marker, and malondialdehyde (MDA) were analyzed. Likewise, subacute toxicity parameters were analyzed. Immunohistochemistry (IHC) and histopathology (H&E/Masson’s trichrome staining) of brain, heart, and pancreatic tissues were done. ECG pattern of all groups was observed. HD-AlCl3 was associated with elevated levels of inflammatory biomarkers, MDA, and glycemic and lipid profiles, whereas it decreased the insulin levels. HD-NaN3 also showed the similar effects of aggravated inflammatory biomarkers, impaired glycemic and lipid profiles, but depicted the maximum mortality rate as compared to HD-AlCl3. IHC showed prominent amyloid plaques and neurofibrillary tangle formation with MD-AlCl3 and HD-AlCl3 as compared to NaN3-treated groups. Likewise, in brain tissues, vacuolation of white matter, vascular congestion, and hemorrhage were seen in HD-AlCl3 treated group, while HD-NaN3 induced death in animals. AlCl3 exposure resulted in an inverted QRS complex, while exposure to NaN3 showed ST depression but with increased mortality. AlCl3 has better controlled results as compared to NaN3 for induction of comorbid experimental animal model depicting early neuroinflammation and cardiometabolic disruption. These determined efforts facilitate the researchers for the development of clinically effective treatment strategies using such experimental models.

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Nattokinase attenuates bisphenol A or gamma irradiation-mediated hepatic and neural toxicity by activation of Nrf2 and suppression of inflammatory mediators in rats

Elbakry

Mansour

Helal

et al. 2022

Environ Sci Pollut Res

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Nattokinase (NK), a protease enzyme produced by Bacillus subtilis, has various biological effects such as lipid-lowering activity, antihypertensive, antiplatelet/anticoagulant, and neuroprotective effects. Exposure to environmental toxicants such as bisphenol A (BPA) or γ-radiation (IR) causes multi-organ toxicity through several mechanisms such as impairment of oxidative status, signaling pathways, and hepatic and neuronal functions as well as disruption of the inflammatory responses. Therefore, this study is designed to evaluate the ameliorative effect of NK against BPA- or IR-induced liver and brain damage in rats. Serum ammonia level and liver function tests were measured in addition to brain oxidative stress markers, amyloid-beta, tau protein, and neuroinflammatory mediators. Moreover, relative quantification of brain nuclear factor-erythroid 2-related factor-2 (Nrf2)/heme oxygenase-1 (HO-1) genes, as well as apoptotic markers in brain tissue, was carried out in addition to histopathological examination. The results showed that NK improved liver functions, impaired oxidative status, the cholinergic deficits, and minified the misfolded proteins aggregates. Furthermore, NK alleviated the neuroinflammation via modulating NF-κB/Nrf2/HO-1 pathway and glial cell activation in addition to their antiapoptotic effect. Collectively, the current results revealed the protective effect of NK against hepatic and neurotoxicity derived from BPA or IR.

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Evaluation of Glucosamine Effect Against Heart and Brain Damage Induced by Y-radiation or Aluminium Chloride in Female Rats

Cited by 4 publications

References 63 publications

Evaluation of Glycogen Synthase Kinase Pathway for Assessing the Antidepressant-like Effect of Glucosamine as a Radioprotector in Rats: Behavioral and Biochemical Studies

Evaluation of Glycogen Synthase Kinase Pathway for Assessing the Antidepressant-like Effect of Glucosamine as a Radioprotector in Rats: Behavioral and Biochemical Studies

Comparative Biochemical Profiling of Aluminum Chloride and Sodium Azide Induced Neuroinflammation and Cardiometabolic Disturbance

Nattokinase attenuates bisphenol A or gamma irradiation-mediated hepatic and neural toxicity by activation of Nrf2 and suppression of inflammatory mediators in rats

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