scholarly journals Effects Of Goat Milk On Memory Performance, Oxidative Status And Neurotrophic Factors In D-Galactose-Induced Ageing Rat Model

2019 ◽  
Author(s):  
Khairunnuur Fairuz Azman ◽  
2020 ◽  
Vol 7 (1) ◽  
pp. 3563-3571
Author(s):  
Afifa Safdar ◽  
Khairunnuur Fairuz Azman ◽  
Rahimah Zakaria ◽  
Che Badariah Ab Aziz ◽  
Usman Rashid

Introduction: Aging is a physiological process accompanied by cognitive decline, particularly in memory deterioration. D-galactose is a reducing monosaccharide which, if systemically exposed, causes accelerated senescence in several organs and is widely being used as an ideal agent to induce brain aging in animal models. Goat milk is a food of high nutritional value which has been demonstrated to possess strong antioxidant and anti-inflammatory properties. However, thus far, little is known of its possible effects on the brain, especially on memory during aging. The present study examined the efficiency of goat milk supplementation on memory performance in a D-galactose induced aging rat model. Methods: Fifty-two male Sprague Dawley rats were randomly divided into four groups: 1) control group, 2) goat milk treated group, 3) D-galactose treated group, and 4) goat milk plus D-galactose treated group. D-galactose (120 mg/kg subcutaneously) and/or goat milk (1 g/kg orally) were administered continuously for six weeks, preceded and followed by novel object recognition and T-maze tests. Results: Prior to goat milk and D-galactose administration, there was no significant difference (p>0.05) in memory performance among all groups. Six weeks of D-galactose administration significantly decreased (p<0.001) short-term, long-term and spatial memory performance. Goat milk supplementation in the D-galactose induced rats managed to protect against memory decline, as exhibited by significantly higher (p<0.0001) short-term, long-term and spatial memory performance of the D-galactose plus goat milk treated group, compared to the D-galactose treated group. Conclusion: In conclusion, goat milk possesses memoryenhancing effects and, hence. may be useful in protecting against age-related memory deficits.  


2018 ◽  
Vol Volume 11 ◽  
pp. 2663-2674 ◽  
Author(s):  
Baowen Liu ◽  
Yi Liu ◽  
Ningbo Li ◽  
Jin Zhang ◽  
Xianwei Zhang

2014 ◽  
Vol 87 (3) ◽  
pp. 177-181 ◽  
Author(s):  
Carina Culic ◽  
Alina Elena Parvu ◽  
Sandu Florin Alb ◽  
Camelia Alb ◽  
Angela Pop

Background and aims. Periodontitis is a chronic inflammation that involves nitro-oxidative stress with damaging periodontal structural effects. We aimed to evaluate the consequences of low-dose cimetidine on nitro-oxidative stress in periodontitis. Methods. A rat model of ligature-induced periodontitis was used. After two weeks, the periodontitis groups were treated with cimetidine, aminoguanidine, N-nitro-L-arginine methyl ester and trolox for one week. On day 21, blood was drawn and the serum analyzed for measurement of total nitrites and nitrates, total oxidative status, total antioxidant response, and oxidative stress index. Results. Cimetidine had an inhibitory effect on the synthesis of nitric oxide (p=0.001), total oxidative status (p=0.01) and oxidative stress index (p=0.01). Total antioxidant reactivity was increased by cimetidine (p=0.01). The effects of cimetidine were almost like those of aminoguanidine, NG-nitro-L-arginine methyl ester, and trolox. Conclusions. Low-dose cimetidine can be used as adjunctive host modulatory therapy in chronic periodontitis because it reduces nitro-oxidative stress.


2017 ◽  
Vol 35 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Fatemeh Sabbaghziarani ◽  
Keywan Mortezaee ◽  
Mohammad Akbari ◽  
Iraj Ragerdi Kashani ◽  
Mansooreh Soleimani ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Mouna Abdelrahman Abujazia ◽  
Norliza Muhammad ◽  
Ahmad Nazrun Shuid ◽  
Ima Nirwana Soelaiman

Virgin coconut oil (VCO) was found to have antioxidant property due to its high polyphenol content. The aim of this study was to investigate the effect of the virgin coconut oil on lipid peroxidation in the bone of an osteoporotic rat model. Normal female Sprague-Dawley rats aged 3 months old were randomly divided into 4 groups, with 8 rats in each group: baseline, sham, ovariectomised (OVX) control group, and OVX given 8% VCO in the diet for six weeks. The oxidative status of the bone was assessed by measuring the index of lipid peroxidation, which is malondialdehyde (MDA) concentration, as well as the endogenous antioxidant enzymes glutathione peroxidase (GPX) and superoxide dismutase (SOD) in the tibia at the end of the study. The results showed that there was a significant decrease in MDA levels in the OVX-VCO group compared to control group. Ovariectomised rats treated with VCO also had significantly higher GPX concentration. The SOD level seemed to be increased in the OVX-VCO group compared to OVX-control group. In conclusion, VCO prevented lipid peroxidation and increased the antioxidant enzymes in the osteoporotic rat model.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Feng He ◽  
Yan-Ping Cao ◽  
Feng-Yuan Che ◽  
Lian-Hong Yang ◽  
Song-Hua Xiao ◽  
...  

Amyloid protein can damage nerve cells through a variety of biological mechanisms including oxidative stress, alterations in calcium homeostasis, and proapoptosis. Edaravone, a potent free radical scavenger possessing antioxidant effects, has been proved neuroprotective effect in stroke patients. The current study aimed to investigate the effects of EDA in an Aβ-induced rat model of AD, by studying Aβ1–40-induced voltage-gated calcium channel currents in hippocampal CA1 pyramidal neurons, learning and memory behavioral tests, the number of surviving cholinergic neurons in the basal forebrain, and the acetylcholine level in the hippocampus in this rat model of AD. The results showed that the Aβ1–40-induced increase ofICacan be inhibited by EDA in a dose-dependent manner. Treatment with EDA significantly improved Aβ1–40-induced learning and memory performance. Choline acetyltransferase positive cells in basal forebrain and acetylcholine content in the hippocampus were increased by the administration of EDA as compared with the non-EDA treated Aβ1–40group. These results demonstrate that EDA can inhibit the neurotoxic effect of Aβtoxicity. Collectively, these findings suggest that EDA may serve as a potential complemental treatment strategy for AD.


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