Metabolic activity of the nervous systen. III. On the amount of non-protein nitrogen in the brain of albino rats during twenty-four hours after feeding

1919 ◽  
Vol 30 (5) ◽  
pp. 396-410 ◽  
Author(s):  
Shigeyuki Komine
2021 ◽  
Vol 22 (8) ◽  
pp. 3829
Author(s):  
Mohamed F. Dora ◽  
Nabil M. Taha ◽  
Mohamed A. Lebda ◽  
Aml E. Hashem ◽  
Mohamed S. Elfeky ◽  
...  

Iron oxide nanoparticle (IONP) therapy has diverse health benefits but high doses or prolonged therapy might induce oxidative cellular injuries especially in the brain. Therefore, we conducted the current study to investigate the protective role of quercetin supplementation against the oxidative alterations induced in the brains of rats due to IONPs. Forty adult male albino rats were allocated into equal five groups; the control received a normal basal diet, the IONP group was intraperitoneally injected with IONPs of 50 mg/kg body weight (B.W.) and quercetin-treated groups had IONPs + Q25, IONPs + Q50 and IONPs + Q100 that were orally supplanted with quercetin by doses of 25, 50 and 100 mg quercetin/kg B.W. daily, respectively, administrated with the same dose of IONPs for 30 days. IONPs induced significant increases in malondialdehyde (MDA) and significantly decreased reduced glutathione (GSH) and oxidized glutathione (GSSG). Consequently, IONPs significantly induced severe brain tissue injuries due to the iron deposition leading to oxidative alterations with significant increases in brain creatine phosphokinase (CPK) and acetylcholinesterase (AChE). Furthermore, IONPs induced significant reductions in brain epinephrine, serotonin and melatonin with the downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and mitochondrial transcription factor A (mtTFA) mRNA expressions. IONPs induced apoptosis in the brain monitored by increases in caspase 3 and decreases in B-cell lymphoma 2 (Bcl2) expression levels. Quercetin supplementation notably defeated brain oxidative damages and in a dose-dependent manner. Therefore, quercetin supplementation during IONPs is highly recommended to gain the benefits of IONPs with fewer health hazards.


Author(s):  
Anne A. Adeyanju ◽  
Folake O. Asejeje ◽  
Olorunfemi R. Molehin ◽  
Olatunde Owoeye ◽  
Esther O. Olatoye ◽  
...  

Abstract Objectives Protocatechuic acid (PCA) possesses numerous pharmacological activities, including antioxidative and anti-inflammatory activities. This study seeks to investigate its underlying mechanism of action in the liver and brain toxicity induced by CCl4 in male albino rats. Methods Rats were given PCA at 10 and 20 mg/kg daily and orally as a pretreatment for seven days. A single injection of CCl4 was given 2 h later to induce brain and liver toxicity. Results CCl4 moderately elevated the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). PCA lowered AST level significantly when compared to control. Total protein and albumin levels presented insignificant changes (p>0.05) in all groups while lipid profile showed increased total cholesterol level and reduced high-density lipoprotein (HDL) by CCl4. PCA (10 mg/kg) significantly reduced the cholesterol level while the 20 mg/kg dose moderately prevented HDL reduction. There was an increased MDA production with a corresponding low GSH level in the group treated with CCl4. Activities of superoxide dismutase, catalase, and glutathione-S-transferase in both organs also declined. PCA, especially at 10 mg/kg attenuated lipid peroxidation by increasing GSH level in the organs. Biochemical assays revealed the improvement of antioxidant enzyme activities by PCA in these organs. Furthermore, PCA lowered the level of proinflammatory cytokine COX 2 in the brain and liver while NF-kB expression was inhibited in the brain. Histopathology reports validated the effects of PCA. Conclusions PCA exhibited protection against toxicity in these tissues through antioxidant and anti-inflammatory activities and the potential mechanism might be through modulation of the NF-κB/COX-2 pathway.


2021 ◽  
Vol 20 (2) ◽  
pp. 37-50
Author(s):  
Joseph S. Ashidi ◽  
Irene. E. Emeya ◽  
Folarin O. Owagboriaye ◽  
Roseline T. Feyisola ◽  
Olubukola I. Lawal ◽  
...  

There has been an increasing rate of cannabis consumption globally, especially among the youths. This study therefore evaluated the neurological behaviours and some brain marker hormones and enzymes of cannabis administered rats. Twenty six albino rats were divided into four groups based on oral cannabis administration (control, Cannabis sativa, Cannabis indica and the combination of the two). At the end of seven days, open field test was conducted on the rats. Also, brain neuro-chemicals, activities of antioxidant enzymes and lipid peroxidation were evaluated using spectrophotometry. The results of the Open-Field Test showed an appreciable increase in the level of ambulation (line crossing), grooming, urination and stretched attend posture in the rats administered with Cannabis indica, Cannabis sativa and the combination when compared with the control. Norepinephrine was significantly lower (p < 0.05) in the rat groups administered with the combination of Cannabis indica and Cannabis sativa. The control group however had the lowest dopamine level. Superoxide dismutase (SOD) was significantly lower (p < 0.05) in the rats administered the combination of both Cannabis indica and Cannabis sativa. The brain level of reduced glutathione (GSH) was significantly higher in the rats administered with Cannabis indica. Malondialdehyde (MDA) was significantly higher in the rats administered with Cannabis sativa than the other rat groups. Histopathological evaluation of the brain also revealed various damages in the brain cells of rats administered with cannabis compared to the normal brain structure of the control rats. It is thus said that consumption of C. sativa or C. indica alone produced mild effect on the brain cells and physiology in rats. However, combination of C. sativa and C. indica produced a severe synergistic effect on the neurological function of the exposed rat.


QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
S S I Elkilany ◽  
M M A Zakaria ◽  
R F Tash ◽  
A Y Mostafa ◽  
S W Abdelmalik ◽  
...  

Abstract Background The importance of sleep and the impact of its deprivation on development of brain pathology became a recent subject of interest in medicine. The restorative effect of sleep on the brain and the harmful effects of insomnia have been recently revealed through the discovery of the glymphatic system and its association with sleep. Aim of work Specific objectives are: To detect histological and apoptotic changes in the neurons and dendrites of the cornu Amonis and the dentate gyrus in sleep deprived rats in comparison to rats with undisturbed sleep pattern (control). To detect deposition of neurotoxic metabolites in comu Amonis and dentate gyrus in sleep deprived rats in comparison to controls. Methods Twenty four adult male Albino rats were used in the present experiment. randomly categorized into four equal groups; Group A1 served as the control group, Group .A2 one day sleep deprivation, Group A3 three days sleep deprivation and Group A4 seven days sleep deprivation. They were deprived of sleep using grid over water method where the animals placed over a grid suspended above tank filled with water with free access to food (rat chew) and water. Hippocampai specimens were collected, processed for paraffin blocks and examined by light microscopy. Results there were neurodegenerative signs appeared from day one sleep deprivation, increased by day three and prevailed by day seven. It was confirmed by apoptotic changes detected by caspase 3 immunohistochemical staining. Furthermore, deposition of beta amyloid appeared in rats deprived of sleep and confirmed by congo red stain. Conclusion Adequate sleep is essential for integrity of the newly discovered glymphatic system responsible for clearance of the brain from waste products including the area most involved in learning and memory function; the hippocampus. Correction of SD could be a viable therapeutic strategy to prevent the onset or slow the progression of AD. Recommendations Further characterization of the glymphatic system in humans are required, it may lead to new therapies and methods of prevention of neurodegenerative diseases. Correction of SD could be a viable therapeutic strategy to prevent the onset or slow the progression of AD.


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