Agmatine, an endogenous ligand of imidazoline receptor protects against memory impairment and biochemical alterations in streptozotocin-induced diabetic rats

Author(s):  
Pravinkumar Bhutada ◽  
Yogita Mundhada ◽  
Vishwas Humane ◽  
Anand Rahigude ◽  
Prashant Deshmukh ◽  
...  
Planta Medica ◽  
2008 ◽  
Vol 74 (09) ◽  
Author(s):  
DK Rai ◽  
PK Rai ◽  
B Sharma ◽  
G Watal

Toxin Reviews ◽  
2019 ◽  
pp. 1-8 ◽  
Author(s):  
Asieh Karimani ◽  
Hossein Hosseinzadeh ◽  
Soghra Mehri ◽  
Amir Hossein Jafarian ◽  
Seyed Akbar Kamali ◽  
...  

Author(s):  
Solaiman Bafadam ◽  
Farimah Beheshti ◽  
Tayebeh Khodabakhshi ◽  
Amir Asghari ◽  
Babak Ebrahimi ◽  
...  

Abstract Background The antidiabetic and antioxidant effects of Trigonella foenum-graceum have been suggested. The effects of hydroalcoholic extract of the plant seeds and metformin against the diabetes-induced memory impairment were investigated. Materials and methods The rats were treated: (1) control, (2) diabetic (3–6) and diabetic rats treated by 50, 100 and 200 mg/kg of the plant extract or metformin. The rats were diabetic by streptozotocin (STZ, 55 mg/kg). After the passive avoidance test, malondialdehyde (MDA), nitric oxide (NO) metabolites, total thiol (SH), catalase (CAT) and superoxide dismutase (SOD) were determined in the brain. Results In the diabetic group, at 3, 24 and 48 h after receiving a shock, the latency to enter the dark room was lower than for the controls (p < 0.001). All doses of the extract and metformin increased the latencies to enter the dark at 3 and 24 h after the shock treatment (p < 0.05–p < 0.001). Additionally, the two higher doses of the extract and metformin increased the latency at 48 h after the shock (p < 0.05–p < 0.001). Diabetes also elevated MDA and NO metabolites, while it reduced thiol, SOD and CAT in the hippocampal and cortical tissues (p < 0.001). Treatment of the diabetic animals by the highest dose of the extract and also metformin reduced the MDA and NO metabolites, while it improved thiols, SOD and CAT (p < 0.01–p < 0.001). Conclusions Based on our findings, metformin and the hydro-alcoholic extract from the T. foenum-graceum seed prevented memory deficits resulting from diabetes. Preventing oxidative damage in the brain may at least, in part, be responsible for the positive effects of the extract and metformin.


2021 ◽  
Vol 10 (3) ◽  
pp. e14510313169
Author(s):  
Aluísio Eustáquio de Freitas Miranda Filho ◽  
Ana Carolina Guimarães Ribeiro ◽  
Nadine Francine Marcula Linhares Nunes ◽  
Samuel Nuno Pereira Lima ◽  
Vinicio Felipe Brasil Rocha ◽  
...  

Secondary disorders in consequences to diabetes involves the development of several diseases in the oral cavity, as periodontitis, xerostomy, infection by diverse pathogens and dysfunctions on the salivary secretion. These alterations occur partially, in consequence of the oxidative stress occasioned by hyperglycemia, and are important in patients undiagnosed or that have flaws in their therapeutic process. The aim of this work was to evaluate biochemical alterations of submandibular glands in response to oxidative stress during diabetes mellitus, and verify the effects of N-acetylcystein supplementation to diabetic rats, specially on the regulation of modifications related to glutathione and thiol proteins. For this purpose, the levels of some oxidative stress markers and the occurrence of the post-translational event of S-glutathionylation were evaluated. The a-amilase degranulation by isolated acinar cells and glandular relative weight was also measured for each experimental group. The compound was able to decrease the lipoperoxidation and proteic oxidation observed in the submandibular gland of diabetic rats, preventing the decrease of the tecidual reducing power and increasing the occurrence of the post-translational process of S-glutathionylation. The diabetic condition increases the degranulation of a-amilase and the glandular weight, but the supplementation with N-acetylcystein did not affect these events. Together these findings may help to elucidate the status of oxidative stress on salivary glands and suggest new therapeutic strategies employing antioxidants of low molecular weight to prevent oral and systemic dysfunctions related to diabetes.


Author(s):  
Shruti Jaiswal ◽  
Torgal Ss ◽  
Sanjay Mishra

 Objective: The present study was designed to evaluate the protective effects of epalrestat (EPS) on memory and learning in type-2 diabetes.Methods: Sixty percent high-fat diet for 2 weeks and a single dose of streptozotocin (35 mg/kg, ip) was used to induce memory impairment in rats. Once the diabetes is confirmed, test drug (EPS - 13.5, 27, and 54 mg/kg, oral) and donepezil (1 mg/kg, oral) were administered to different groups of rats for 4 weeks followed by an assessment of memory and learning deficit using behavioral paradigms: Elevated plus maze (EPM), Morris water maze (MWM), and passive avoidance test.Results: EPS and donepezil showed significant improvement in learning and memory of rats, as indicated by markedly decreased escape latency to reach a hidden platform and increased time spent in target quadrant using MWM task, reduced transfer latency in EPM, and also there is a significant increase in the transfer latencies using passive avoidance test were noted. Memory-enhancing activity of EPS (13.5, 27, and 54 mg/kg) was comparable with the diabetic control group.Conclusion: The study findings suggest that memory-enhancing effect of EPS may be mediated by its antioxidant and anti-inflammatory activities. This recommends the potential effect of EPS therapy as a useful memory restorative agent in the treatment of neurodegenerative disease seen in type-2 diabetes rat.


2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Saleh A. Bakheet ◽  
Sabry M. Attia

We used the bone marrow DNA strand breaks, micronucleus formations, spermatocyte chromosomal aberrations, and sperm characteristic assays to investigate the chromosomal instability in somatic and germinal cells of diabetic rats treated with multiple doses of naringin. The obtained results revealed that naringin was neither cytotoxic nor genotoxic for the rats at all tested doses. Moreover, naringin significantly reduced the diabetes-induced chromosomal instability in somatic and germinal cells in a dose-dependent manner. In addition, diabetes induced marked biochemical alterations characteristic of oxidative stress including enhanced lipid peroxidation, accumulation of oxidized glutathione, reduction in reduced glutathione, and accumulation of intracellular reactive oxygen species. Treatment with naringin ameliorated these biochemical markers dose-dependently. In conclusion, naringin confers an appealing protective effect against diabetes-induced chromosomal instability towards rat somatic and germinal cells which might be explained partially via diminishing thede novofree radical generation induced by hyperglycemia. Thus, naringin might be a good candidate to reduce genotoxic risk associated with hyperglycemia and may provide decreases in the development of secondary malignancy and abnormal reproductive outcomes risks, which seems especially important for diabetic patients.


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