scholarly journals Folic acid attenuated learning and memory impairment via inhibition of oxidative damage and acetylcholinesterase activity in hypothyroid rats

2021 ◽  
Author(s):  
Sabiheh Amirahmadi ◽  
Mahmoud Hosseini ◽  
Somaieh Ahmadabady ◽  
Mahsan Akbarian ◽  
Kataneh Abrari ◽  
...  
Keyword(s):  
Folic Acid ◽  
Oxidative Damage ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Acetylcholinesterase Activity

scholarly journals Folic Acid Attenuated Learning and Memory Impairment via Inhibition of Oxidative Damage and Acetylcholinesterase Activity in Hypothyroid Rats

2021 ◽  
Author(s):  
Sabiheh Amirahmadi ◽  
Mahmoud Hosseini ◽  
Somaieh Ahmadabady ◽  
Mahsa Akbarain ◽  
Kataneh Abrari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Oxidative Damage ◽  
Learning And Memory ◽  
Cognitive Performance ◽  
Ache Activity ◽  
Acetylcholinesterase Activity ◽  
Protective Effects ◽  
Thiol Content ◽  
Oxidative Stress Indicators

Abstract Hypothyroidism has been associated with cognitive decline. Considering the role that has been suggested for folic acid (FA) in cognitive performance, the present study was designed to investigate the effects of FA against hypothyroidism-induced cognitive impairment, oxidative damage and acetylcholinesterase (AChE) activity alterations in propylthiouracil (PTU)-induced hypothyroid rats. In this study, PTU (0.05% in drinking water) and FA (5, 10, and 15 mg/kg, oral gavage) were administered to the rats for a period of 7 weeks. Then, behavioral performance was tested using Morris water maze (MWM) and passive avoidance (PA) tasks. Finally, oxidative stress indicators and AChE activity were assayed in the brain tissues. The impairing effect of hypothyroidism on cognitive performance was markedly alleviated by FA especially at the higher doses. In the MWM test, FA reduced escape latency and travelled distance, compared to the non-treated hypothyroid group. In the PA test, the latency to enter the dark chamber was significantly enhanced by FA as compared to the non-treated hypothyroid group (p < 0.05-p < 0.001). Besides, FA attenuated AChE activity and malondialdehyde level but increased superoxidase dismutase enzyme activity and total thiol content (p < 0.05-p < 0.001). In conclusion, FA could improve learning and memory ability in hypothyroid rats. The observed protective effects may be mediated through regulation of oxidative stress and AChE activity.

Effects of PPAR-γ agonist, pioglitazone on brain tissues oxidative damage and learning and memory impairment in juvenile hypothyroid rats

2019 ◽  
Vol 129 (10) ◽  
pp. 1024-1038 ◽  
Author(s):  
Yousef Baghcheghi ◽  
Hossein Salmani ◽  
Farimah Beheshti ◽  
Mohammad Naser Shafei ◽  
Hamid Reza Sadeghnia ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Ppar Γ ◽  
Brain Tissues

scholarly journals Neuroprotective Effects ofCentella asiaticaagainst Intracerebroventricular Colchicine-Induced Cognitive Impairment and Oxidative Stress

2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Anil Kumar ◽  
Samrita Dogra ◽  
Atish Prakash
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Oxidative Damage ◽  
Memory Impairment ◽  
Memory Performance ◽  
Centella Asiatica ◽  
Acetylcholinesterase Activity ◽  
Early Event ◽  
Neuroprotective Effects ◽  
Male Wistar Rats

Oxidative stress appears to be an early event involved in the pathogenesis of Alzheimer's disease. The present study was designed to investigate the neuroprotective effects ofCentella asiaticaagainst colchicine-induced memory impairment and oxidative damage in rats. Colchicine (15 μg/5 μL) was administered intracerebroventricularly in the lateral ventricle of male wistar rats. Morris water maze and plus-maze performance tests were used to assess memory performance tasks. Various biochemical parameters such as lipid peroxidation, nitrite, reduced glutathione, glutathione-S-transferase, superoxide dismutase, acetylcholinesterase were also assessed. ICV colchicine resulted marked memory impairment and oxidative damage. Chronic treatment withCentella asiaticaextract (150 and 300 mg/kg, p.o.) for a period of 25 days, beginning 4 days prior to colchicine administration, significantly attenuated colchicine-induced memory impairment and oxidative damage. Besides,Centella asiaticasignificantly reversed colchicines administered increase in acetylcholinesterase activity. Thus, present study indicates protective effect ofCentella asiaticaagainst colchicine-induced cognitive impairment and associated oxidative damage.

Ameliorative Potential of Glycyrrhiza glabra extracts on Memory Impairments in Stress Triggered Rats

2020 ◽  
Vol 06 ◽  
Author(s):  
Parul Kamboj ◽  
Ajit Kumar Thakur
Keyword(s):  
Antioxidant Enzyme ◽  
Learning And Memory ◽  
Acetylcholinesterase Activity ◽  
Molecular Study ◽  
Glycyrrhiza Glabra ◽  
Learning Ability ◽  
Future Research ◽  
Standard Drug ◽  
Behavioral Alteration ◽  
Memory Enhancing

Background: Glycyrrhiza glabra Linn. (Family: Fabaceae) has been known to very useful medicinal plant in the Traditional Medicinal Systems from the centuries. With ethnopharmacological values, it is well-reported plant for their traditional uses for anti-inflammatory, antioxidant, anxiolytic, expectorant activities, and antidepressant activities. Objective: Although it is described for memory enhancing activity, the present study was focused to examine the comparative effect of Glycyrrhiza glabra extracts viz. flavonoid rich (GGFE) and glycyrrhizin rich (GGGE) in stress triggered rats and to provide future research insight for this herbal drug, for which no scientific justification has been reported till now. Methods: Male Wister rats divided into 7 different groups (n= 6 per group) were given chronic foot-shock stress for 21 successive days with scheduled administration of the extracts (50 and 100 mg/kg) and standard drug (10 mg/kg) for 28 days. Elevated Plus Maze, Rectangular Maze, Morris Water Maze, and Locomotor activity were performed to test behavioral alteration and learning ability of stressed rats. Further, rats were sacrificed to assay acetylcholinesterase activity and antioxidant activity in brain samples for the mechanistic role in learning and memory. Results: Extracts of Glycyrrhiza glabra were indicated a significant alteration in stress induced learning and memory deficiency in behavioral parameters studied. These extracts were also modulated significant changes in acetylcholinesterase and antioxidant enzyme activity to improve the learning and memory of stressed rats. Conclusions: It is concluded that both extracts of Glycyrrhiza glabra (GGFE and GGGE) possess memory enhancing property in stress triggered rats. Moreover, these comparative results provided information and confirmed the high potential of GGGE in comparison to GGFE might be due to rich glycyrrhizin content present in GGGE responsible for acetylcholinesterase and antioxidant enzyme modulatory activity. Therefore, GGGE could be used as a promising lead for further mechanistic and molecular study for defining the role of glycyrrhizin of Glycyrrhiza glabra.

scholarly journals Ferroptosis contributes to isoflurane-induced neurotoxicity and learning and memory impairment

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Pengfei Liu ◽  
Jing Yuan ◽  
Yetong Feng ◽  
Xin Chen ◽  
Guangsuo Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Close Association ◽  
Dimethyl Fumarate ◽  
Dependent Manner ◽  
Transport Chain ◽  
The Relationship

AbstractFerroptosis is a novel type of programmed cell death, which is different from apoptosis and autophagic cell death. Recently, ferroptosis has been indicated to contribute to the in vitro neurotoxicity induced by isoflurane, which is one of the most common anesthetics in clinic. However, the in vivo position of ferroptosis in isoflurane-induced neurotoxicity as well as learning and memory impairment remains unclear. In this study, we mainly explored the relationship between ferroptosis and isoflurane-induced learning and memory, as well as the therapeutic methods in mouse model. Our results indicated that isoflurane induced the ferroptosis in a dose-dependent and time-dependent manner in hippocampus, the organ related with learning and memory ability. In addition, the activity of cytochrome c oxidase/Complex IV in mitochondrial electron transport chain (ETC) was increased by isoflurane, which might further contributed to cysteine deprivation-induced ferroptosis caused by isoflurane exposure. More importantly, isoflurane-induced ferroptosis could be rescued by both ferroptosis inhibitor (ferrostatin-1) and mitochondria activator (dimethyl fumarate), which also showed effective therapeutic action against isoflurane-induced learning and memory impairment. Taken together, our data indicate the close association among ferroptosis, mitochondria and isoflurane, and provide a novel insight into the therapy mode against isoflurane-induced learning and memory impairment.

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