Aluminium chloride 20% spray

Alzheimer's disease (AD) is a chronic neurodegenerative disease categorized by the deficiency in the cognition and memory. Approximately 50 million peoples has the AD, which is categorized by the deficiency in the cognition, memory and other kinds of cognitive dissention. The present exploration was designed to unveil the ameliorative properties of ononin against the aluminium chloride (AlCl3)-provoked AD in animals via the suppression of oxidative stress and neuroinflammation. AD was provoked to the Sprague Dawley rats through administering orally with 0.5 ml/100 g b.wt. of AlCl3 25 days and then supplemented with the 30 mg/kg of ononin orally for 25th day to 36th day. The behavioural changes were examined using open field and Morris Water Maze test. The acetylcholine esterase (AChE) activity was studied by standard method. The status of Aβ1-42, MDA, SOD, total antioxidant capacity (TAC) were quantified using respective assay kits. The interleukin(IL)-1β and TNF-α, BDNF, PPAR-γ, p38MAPK, and NF-κB/p65 status was quantified using respective assay kits. Brain histology was studied using microscope. The ononin treatment effectively modulated the AlCl3-triggered behavioural alterations in the AD animals. Ononin appreciably suppressed the AChE, Aβ1-42, and MDA and improved the SOD and TAC in the brain tissues of AD animals. The status of IL-1β, TNF-α, p38MAPK, and NF-κB were suppressed and the BDNF and PPAR-γ contents were elevated in the brain tissues of AD animals. The outcomes brain histology analysis proved the attenuate role of ononin. Our findings recommended that the ononin treatment could ameliorate the cognitive impairment, suppress the neuroinflammation and oxidative stress in the AD animals.

Abstract licence: CC BY-NC-ND

Alzheimer’s disease (AD) is a major form of dementia among neurodegenerative diseases, which results in memory loss and attention deficits. Syringic acid (SA) is a phenolic compound derivative of plants and fruits, which possessed the numerous biological activities. The present study aims to examine the neuroprotective potential of SA on aluminium chloride (AlCl3) stimulated behavioral deficits and neuroinflammation in the rat AD. The AlCl3 (100 mg/kg.b.wt) via injected intraperitoneally for 60 days to stimulate the AD. The rats were supplemented with low and high doses of SA (25 & 50 mg/kg.b.wt) of SA for 30 days. After end of the experiment, we evaluated behavioral examinations like Morris water maze, Y-maze, elevated plus maze and open field test. Followed by acetylcholinesterase (AChE), biochemical measurement and inflammatory protein expression by western blotting were examined. AD rats displayed reduced memory and learning impairments, augmented short term memory loss and diminished locomotion activity. Interestingly, the neurobehavioral impairments were appreciably stabilized by the SA supplementation to the AD rats. The NF-ƙB, IL-1β, IL-6, and TNF-α expressions were assuaged via the SA supplementation to AD rats. The present work demonstrated that the SA treatment ameliorated the AlCl3 stimulated AD.

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Background: Alzheimer’s disease (AD) is a neurodegenerative disorder and the commonest cause of dementia among the aged people. D-galactose (D-gal) is a senescence agent, while aluminium is a known neurotoxin linked to pathogenesis of AD. The combined administration of rats with d-gal and aluminium chloride (AlCl3) is considered to be an easy and a cheap method to obtain an animal model of AD. The plant Centella asiatica (CA) is reported to exert neuroprotective effects both in vitro and in vivo. Therefore, this study explored the protective effects of CA on cognition and brain ultrastructure in d-gal and AlCl3 induced rats. Materials and methods: Rats were exposed to d-gal 60 mg/kg/b.wt/day + AlCl3 200 mg/kg/b.wt/day and CA (200, 400 and 800 mg/kg/b.wt/day) and 1 mg/kg/b.wt/day of donepezil for 70 days. Different cognitive paradigms viz. T maze spontaneous alternation, modified elevated plus maze and novel object recognition test, were used to evaluate full lesions of the hippocampus, spatial learning and memory and non-spatial learning and memory respectively. Nissl’s staining was used to determine the survival of hippocampus CA1 pyramidal cells, while transmission electron microscopy was used to check the ultrastructural changes. Results: The results revealed that d-gal and AlCl3 could significantly impair behavior and cognitive functions, besides causing damage to the hippocampal CA1 pyramidal neurons in rats. In addition, it also caused ultrastructural morphological alterations in rat hippocampus. Conversely, co-administration o;f CA, irrespective of the dosage used, alleviated the cognitive impairments and pathological changes in the rats comparable to donepezil. Conclusion: In conclusion the results suggest that CA could protect cognitive impairments and morphological alterations caused by d-gal and AlCl3 toxicity in rats. Biochemical and molecular studies are ongoing to elucidate the probable pharmacodynamics of CA.

Abstract licence: CC BY-NC-ND

Alzheimer's disease (AD) is the most common form of dementia that mainly affects the cognitive functions of the aged populations. Trigonella foenum-graecum (L.) (fenugreek), a traditionally well utilized medicinal plant ubiquitously used as one of the main food additive worldwide, is known to have numerous beneficial health effects. Fenugreek seed extract could be able to inhibit the activity of acetylcholinesterase (AChE), a key enzyme involved in the pathogenesis of AD, and further shown to have anti-parkinsonic effect. The present study was aimed to explore the neuroprotective effect of fenugreek seed powder (FSP) against aluminium chloride (AlCl3) induced experimental AD model. Administration of germinated FSP (2.5, 5 and 10% mixed with ground standard rat feed) protected AlCl3 induced memory and learning impairments, Al overload, AChE hyperactivity, amyloid β (Aβ) burden and apoptosis via activating Akt/GSK3β pathway. Our present data could confirm the neuroprotective effect of fenugreek seeds. Further these results could lead a possible therapeutics for the management of neurodegenerative diseases including AD in future.

Abstract licence: CC BY

Aluminium is known to accelerate oxidative stress, amyloid beta (A β ) deposition, and plaque formation in the brain of rats. Objective . The present study is aimed at studying the neuroprotective effects of eugenol following aluminium-induced neurotoxicity on caspase-3, apoptotic proteins (Bcl-2 and Bax), and oxidative stress markers in Wistar rats such as superoxide dismutase (SOD), glutathione peroxidase (GPx), nitric oxide (NO), and assay oxidative stress to mitochondrial DNA (mtDNA) by measuring the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG). Materials and methods . Twenty (20) adult Wistar rats were randomly divided into four (4) groups with five animals in each group. Route of administration was oral throughout the duration of this study and this study lasted for 21 days. Rats were sacrificed 24 hours after administration of the last dose (i.e., day 22) with 0.8 mg/kg ketamine as an anaesthetic agent. Results . Exposure to AlCl 3 resulted in a significant (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mi>p</mml:mi><mml:mo>&lt;</mml:mo><mml:mn>0.01</mml:mn></mml:math>) elevation in the levels of nitric oxide and 8-hydroxy-2-deoxyguanosine (8-OHdG), enhanced the activity of caspase-3, increased the level of proapoptotic protein Bax and reduced the levels of antiapoptotic protein Bcl-2, and significantly (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mi>p</mml:mi><mml:mo>&lt;</mml:mo><mml:mn>0.01</mml:mn></mml:math>) reduced the levels of SOD and GPx. However, treatment with eugenol resulted in a significant reduction (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M3"><mml:mi>p</mml:mi><mml:mo>&lt;</mml:mo><mml:mn>0.01</mml:mn></mml:math>) in the levels of nitric oxide (NO) and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, inhibited the activity of caspase-3, increased levels of Bcl-2 and significantly (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M4"><mml:mi>p</mml:mi><mml:mo>&lt;</mml:mo><mml:mn>0.05</mml:mn></mml:math>) reduced levels of Bax protein, respectively, and also significantly (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M5"><mml:mi>p</mml:mi><mml:mo>&lt;</mml:mo><mml:mn>0.05</mml:mn></mml:math>) increased the levels of SOD and GPx. Our results would hereby suggest that eugenol would provide a therapeutic value against aluminium-induced oxidative stress as related to antioxidant and antiapoptotic activities.

Abstract licence: CC BY