scholarly journals The Effect of Kaempferol on Autophagy and Nrf-2 Signaling in a Rat Model of Aβ1-42-induced Alzheimer’s Disease

2022 ◽  
Vol 8 (1) ◽  
pp. 7-16
Author(s):  
Adeleh Jafari ◽  
◽  
Parvin Babaei ◽  
Kambiz Rohampour ◽  
Samira Rashtiani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Passive Avoidance ◽  
Rat Model ◽  
Natural Antioxidants ◽  
Beclin 1 ◽  
Key Factor ◽  
Male Wistar Rats ◽  
Avoidance Memory

Background: Numerous pieces of evidence support that oxidative stress is a key factor in the pathogenesis of neurodegenerative diseases, like Alzheimer’s Disease (AD). Suppression of oxidative stress is an attractive strategy and flavonoids as potent natural antioxidants are extremely noticeable. Objectives: In this study, the effects of Kaempferol (KMP) were evaluated on passive avoidance memory, hippocampal Nrf-2, and beclin-1 expression in a rat model of Aβ1-42 –induced AD. Materials & Methods: Forty male Wistar rats weighing 200-250 g were divided into five groups (n=8); sham-operated, AD model, and KMP treatment (5, 7.5, 10 mg/kg, i.p. for three weeks). Animals received an intracerebroventricular injection of amyloid-beta (1-42) to establish an AD model. Passive avoidance memory of rats was evaluated using a shuttle box on day 21; Step-Through Latency (STL) and time spent in The Dark Compartment (TDC) were recorded. Then, hippocampus homogenates were used for biochemical and molecular analysis by real-time PCR, western blot, and ELISA. Results: It was found that KMP improved memory evidenced by increased STL (P≤0.05) and decreased TDC (p≤0.01). KMP also increased the levels of Total Antioxidant Capacity (TAC) in the hippocampus of rats (P≤0.05). In addition, KMP enhanced the expression of Nrf-2 mRNA (P≤0.001) and beclin-1 protein in the hippocampus tissues (P≤0.001). Conclusion: Overall, it is suggested that the memory-improving effect of KMP is mediated, at least in part, by enhancing Nrf-2 and TAC. KMP is also able to induce autophagy through the expression of beclin-1.

scholarly journals Dental Pulp Stem Cells Transplantation Improves Passive Avoidance Memory and Neuroinflammation in Trimethyltin-Induced Alzheimer’s Disease Rat Model

2021 ◽  
Vol 10 ◽  
pp. e2254
Author(s):  
Samira Malekzadeh ◽  
Mohammad Amin Edalatmanesh ◽  
Davood Mehrabani ◽  
Mehrdad Shariati
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Serum Level ◽  
Passive Avoidance ◽  
Rat Model ◽  
Dental Pulp ◽  
Dental Pulp Stem Cells ◽  
Dark Compartment ◽  
Avoidance Memory

Background: According to the increasing incidence of Alzheimer’s disease (AD), this study aimed to investigate the effect of dental pulp stem cells (DPSCs) transplantation on passive avoidance memory and neuroinflammation in trimethyltin (TMT)-induced AD rat model. Materials and Methods: In this experimental study, 18 male Wistar rats were randomly divided into three groups: the control that rats received 8 mg/kg TMT plus 0.5 ml phosphate buffered saline (PBS) and TMT+DPSCs (TMT + 1×106 cells/ml DPSC in 0.5 ml PBS) groups. Then, after one month, passive avoidance test was performed. Also measured the Nuclear Factor Kappa-β (NF-Kβ) serum level and the percentage of damaged neurons in the hippocampus were determined. Results: DPSCs transplantation showed significantly increased step-through latency to the dark compartment in comparison with control and TMT+PBS groups in 24 hours after shock. Also, time spent in the dark compartment of TMT+DPSCs significantly decreased compared to control and TMT+PBS groups in 24 and 48 hours after shock (P<0.05). Furthermore, DPSCs transplantation significantly decreased the NF-Kβ serum level and percentage of damaged pyramidal neurons of CA1 compared with TMT+PBS (P<0.05). Conclusion: DPSCs transplantation improved memory and learning, regulated NF-Kβ serum level, and decreased damage neurons of CA1 hippocampus in TMT-induced AD rat model.

scholarly journals Failure of the Brain Glucagon-Like Peptide-1-Mediated Control of Intestinal Redox Homeostasis in a Rat Model of Sporadic Alzheimer’s Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1118
Author(s):  
Jan Homolak ◽  
Ana Babic Perhoc ◽  
Ana Knezovic ◽  
Jelena Osmanovic Barilar ◽  
Melita Salkovic-Petrisic
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Redox Homeostasis ◽  
Brain State ◽  
Gastrointestinal Hormone ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

The gastrointestinal system may be involved in the etiopathogenesis of the insulin-resistant brain state (IRBS) and Alzheimer’s disease (AD). Gastrointestinal hormone glucagon-like peptide-1 (GLP-1) is being explored as a potential therapy as activation of brain GLP-1 receptors (GLP-1R) exerts neuroprotection and controls peripheral metabolism. Intracerebroventricular administration of streptozotocin (STZ-icv) is used to model IRBS and GLP-1 dyshomeostasis seems to be involved in the development of neuropathological changes. The aim was to explore (i) gastrointestinal homeostasis in the STZ-icv model (ii) assess whether the brain GLP-1 is involved in the regulation of gastrointestinal redox homeostasis and (iii) analyze whether brain-gut GLP-1 axis is functional in the STZ-icv animals. Acute intracerebroventricular treatment with exendin-3(9-39)amide was used for pharmacological inhibition of brain GLP-1R in the control and STZ-icv rats, and oxidative stress was assessed in plasma, duodenum and ileum. Acute inhibition of brain GLP-1R increased plasma oxidative stress. TBARS were increased, and low molecular weight thiols (LMWT), protein sulfhydryls (SH), and superoxide dismutase (SOD) were decreased in the duodenum, but not in the ileum of the controls. In the STZ-icv, TBARS and CAT were increased, LMWT and SH were decreased at baseline, and no further increment of oxidative stress was observed upon central GLP-1R inhibition. The presented results indicate that (i) oxidative stress is increased in the duodenum of the STZ-icv rat model of AD, (ii) brain GLP-1R signaling is involved in systemic redox regulation, (iii) brain-gut GLP-1 axis regulates duodenal, but not ileal redox homeostasis, and iv) brain-gut GLP-1 axis is dysfunctional in the STZ-icv model.

Impact of Cerebral Radiofrequency Exposures on Oxidative Stress and Corticosterone in a Rat Model of Alzheimer’s Disease

2020 ◽  
Vol 73 (2) ◽  
pp. 467-476 ◽  
Author(s):  
Marc Bouji ◽  
Anthony Lecomte ◽  
Christelle Gamez ◽  
Kelly Blazy ◽  
Anne-Sophie Villégier
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Model Of Alzheimer’S Disease

Effects of levothyroxine on lung inflammation, oxidative stress and pathology in a rat model of Alzheimer’s disease

2020 ◽  
Vol 277 ◽  
pp. 103437
Author(s):  
Kowsar Bavarsad ◽  
Saeideh Saadat ◽  
Nema Mohammadian Roshan ◽  
Mousa-Al-Reza Hadjzadeh ◽  
Mohammad Hossein Boskabady
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Lung Inflammation ◽  
Model Of Alzheimer’S Disease

Protective Effect of Kaempferol on the Transgenic Drosophila Model of Alzheimer’s Disease

2018 ◽  
Vol 17 (6) ◽  
pp. 421-429 ◽  
Author(s):  
Tanveer Beg ◽  
Smita Jyoti ◽  
Falaq Naz ◽  
Rahul ◽  
Fahad Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Neuronal Damage ◽  
Natural Antioxidants ◽  
Acetylcholinesterase Activity ◽  
Model Of Alzheimer’S Disease ◽  
Climbing Ability ◽  
Transgenic Drosophila

Background: Alzheimer’s disease (AD) is characterized by the accumulation and deposition of β-amyloid peptides leading to a progressive neuronal damage and cell loss. Besides several hypotheses for explaining the neurodegenerative mechanisms, oxidative stress has been considered to be one of them. Till date, there is no cure for AD, but the pathogenesis of the disease could be delayed by the use of natural antioxidants. In this context, we decided to study the effect of kaempferol against the transgenic Drosophila expressing human amyloid beta-42. Method: The AD flies were allowed to feed on the diet having 10, 20, 30 and 40µM of kaempferol for 30 days. After 30 days of exposure, the amyloid beta flies were studied for their climbing ability and Aversive Phototaxis Suppression assay. Amyloid beta flies head homogenate was prepared for estimating the oxidative stress markers, Caspase and acetylcholinesterase activity. Results: The results of the present study reveal that the exposure of AD flies to kaempferol delayed the loss of climbing ability, memory, reduced the oxidative stress and acetylcholinesterase activity. Conclusion: Kaempferol could be used as a possible therapeutic agent against the progression of the Alzheimer’s disease.

scholarly journals Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer's disease.

2011 ◽  
Vol 58 (4) ◽  
Author(s):  
Hanan F Aly ◽  
Fateheya M Metwally ◽  
Hanaa H Ahmed
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Body Weight ◽  
Rat Model ◽  
Neurotrophic Factor ◽  
Intraperitoneal Administration ◽  
Brain Derived Neurotrophic Factor ◽  
Ovariectomized Rats ◽  
Antioxidant Enzyme Activities

The current study was undertaken to elucidate a possible neuroprotective role of dehydroepiandrosterone (DHEA) against the development of Alzheimer's disease in experimental rat model. Alzheimer's disease was produced in young female ovariectomized rats by intraperitoneal administration of AlCl(3) (4.2 mg/kg body weight) daily for 12 weeks. Half of these animals also received orally DHEA (250 mg/kg body weight, three times weekly) for 18 weeks. Control groups of animals received either DHAE alone, or no DHEA, or were not ovariectomized. After such treatment the animals were analyzed for oxidative stress biomarkers such as hydrogen peroxide, nitric oxide and malondialdehyde, total antioxidant capacity, reduced glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase and catalase activities, antiapoptotic marker Bcl-2 and brain derived neurotrophic factor. Also brain cholinergic markers (acetylcholinesterase and acetylcholine) were determined. The results revealed significant increase in oxidative stress parameters associated with significant decrease in the antioxidant enzyme activities in Al-intoxicated ovariectomized rats. Significant depletion in brain Bcl-2 and brain-derived neurotrophic factor levels were also detected. Moreover, significant elevations in brain acetylcholinesterase activity accompanied with significant reduction in acetylcholine level were recorded. Significant amelioration in all investigated parameters was detected as a result of treatment of Al-intoxicated ovariectomized rats with DHEA. These results were confirmed by histological examination of brain sections. These results clearly indicate a neuroprotective effect of DHEA against Alzheimer's disease.

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