Preventive effect of Rubus fruticosus on learning and memory impairment in an experimental model of diabetic neuropathy in male rats

2014 ◽  
Vol 2 (4) ◽  
pp. 155-160 ◽  
Author(s):  
Ali Gomar ◽  
Abdolkarim Hosseini ◽  
Naser Mirazi
2020 ◽  
Vol 14 (4) ◽  
pp. 40-47
Author(s):  
Mehrdad Farivar ◽  
Zahra Hooshmandi ◽  
Mahbubeh Setorki ◽  
Sabrieh Amini ◽  
◽  
...  

2019 ◽  
Vol 8 ◽  
pp. 1182 ◽  
Author(s):  
Solmaz Khalifeh ◽  
Mehdi Khodamoradi ◽  
Vahid Hajali ◽  
Hamed Ghazvini ◽  
Lelia Eliasy ◽  
...  

Background: Methamphetamine (METH) as a synthetic psychostimulant is being increasingly recognized as a worldwide problem, which may induce memory impairment. On the other hand, it is well established that naloxone, an opiate antagonist, has some beneficial effects on learning and memory. The present research aimed at evaluating naloxone effects on spatial learning and memory impairment triggered by a neurotoxic regimen of METH in male rats. Materials and Methods: The animals received the subcutaneous (sc) regimen of METH (4×6 mg/kg at 2-h intervals), intraperitoneal (ip) naloxone (4×1 mg/kg at 2-h intervals), or normal saline at four events. The Nal-METH group of rats received four naloxone injections (1 mg/kg, ip) 30 min before each METH injection (6 mg/kg, sc) at 2-h intervals. Seven days later, they were evaluated for spatial learning and memory in the Morris Water Maze (MWM) task. Result: METH regimen induced hyperthermia, as well as a poor performance, in the acquisition and retention phases of the task, indicating spatial learning and memory impairment compared to the controls. Naloxone administration (1 mg/kg, ip) before each METH injection led to significant attenuations of both hyperthermia and METH adverse effects on the rat performance in the MWM task. Conclusion: The results revealed that pretreatment with the opiate antagonist naloxone could prevent METH adverse effects on body temperature and memory performance. It seems that the opioidergic system and hyperthermia may, at least partially, be involved in METH effects on spatial memory. [GMJ. 2019;8:e1182]


2012 ◽  
Vol 37 (7) ◽  
pp. 1784-1792 ◽  
Author(s):  
Giuseppe D'Agostino ◽  
Roberto Russo ◽  
Carmen Avagliano ◽  
Claudia Cristiano ◽  
Rosaria Meli ◽  
...  

2021 ◽  
Vol 53 ◽  
pp. S623-S624
Author(s):  
M. Georgieva-Kotetarova ◽  
I. Kostadinov ◽  
D. Delev ◽  
H. Zlatanova ◽  
I. Kandilarov ◽  
...  

2016 ◽  
Vol 39 (3) ◽  
pp. 901-907 ◽  
Author(s):  
Gengyin Wang ◽  
Hui Fang ◽  
Yanfeng Zhen ◽  
Gang Xu ◽  
Jinli Tian ◽  
...  

Background/Aims: To explore the effects of sulforaphane (SFN) on neuronal apoptosis in hippocampus and memory impairment in diabetic rats. Methods: Thirty male rats were randomly divided into normal control, diabetic model and SFN treatment groups (N = 10 in each group). Streptozotocin (STZ) was applied to establish diabetic model. Water Morris maze task was applied to test learning and memory. Tunel assaying was used to detect apoptosis in hippocampus. The expressions of Caspase-3 and myeloid cell leukemia 1(MCL-1) were detected by western blotting. Neurotrophic factor levels and AKT/GSK3β pathway were also detected. Results: Compared with normal control, learning and memory were apparently impaired, with up-regulation of Caspase-3 and down-regulation of MCL-1 in diabetic rats. Apoptotic neurons were also found in CA1 region after diabetic modeling. By contrast, SFN treatment prevented the memory impairment, decreased the apoptosis of hippocampal neurons. SFN also attenuated the abnormal expression of Caspase-3 and MCL-1 in diabetic model. Mechanically, SFN treatment reversed diabetic modeling-induced decrease of p-Akt, p-GSK3β, NGF and BDNF expressions. Conclusion: SFN could prevent the memory impairment and apoptosis of hippocampal neurons in diabetic rat. The possible mechanism was related to the regulation of neurotropic factors and Akt/GSK3β pathway.


Sign in / Sign up

Export Citation Format

Share Document