scholarly journals The Protective Effects of Nicotine and Bucladesine on Impaired Avoidance Memory Caused by Sodium Arsenate Toxicity in Mice

2021 ◽  
Vol 15 (2) ◽  
pp. 99-108
Author(s):  
Sheyda Najafi ◽  
◽  
Mahmoud Hashemzaei ◽  
Maryam Sadeghi ◽  
Sajedeh Seyed Mousavi ◽  
...  
Keyword(s):  
Synergistic Effects ◽  
Deionized Water ◽  
Avoidance Task ◽  
Memory Retention ◽  
Protective Effects ◽  
Neuronal Function ◽  
Sodium Arsenate ◽  
Dark Chamber ◽  
Time Latency ◽  
Avoidance Memory

Background: The toxic effect of sodium arsenate on nervous system has been shown; but the protective effects of several compounds against sodium arsenate are not clear. This study aimed to investigate the protective effects of nicotine and bucladesine, two positive modulators of neuronal function, on sodium arsenate toxicity against avoidance memory impairment. Methods: Male mice (N=154) were assigned to 22 groups (12 experimental and 10 control) of seven animals each and were treated as follows: sodium arsenate (2.5, 5, or 10 mg/kg) for 28 days, nicotine (1 mg/kg) for either 1, 2, or 4 days, bucladesine (600 nM/mouse) for either 1, 2, or 4 days, and nicotine (1 mg/kg)+bucladesine (600 nM/mouse)+sodium arsenate (2.5 mg/kg). The last group was treated with 2.5 mg/kg sodium arsenate first, and then received the combination of nicotine and bucladesine for 1, 2, or 4-days. The corresponding control groups did not receive any drug but either saline, deionized water, or combination of deionized water and DMSO, but went through the same procedure as other animals. All mice were trained 24 h in the step-through passive avoidance task. The avoidance memory retention was assessed at 24, 48, 96, and 168 h after the training period by measuring the time they stayed in a dark chamber. Results: All sodium arsenate doses significantly reduced the time stayed in the dark chamber regardless of the treatment duration (24, 48, 96 & 168 h) after training. Both nicotine and bucladesine, whether used singly or combined for 1, 2, and 4 days significantly enhanced the time latency compared to the controls at all of the experimental timepoints following the training. Conclusion: Nicotine and bucladesine showed synergistic effects and reversed the sodium arsenate-induced avoidance memory deficits in mice.

scholarly journals Intersections Of Neighborhood Co-Ethnic Density and Nativity Status On Heavy Drinking In a General Population Sample Of US Latinos and Asians

2020 ◽  
Vol 56 (1) ◽  
pp. 74-81
Author(s):  
Christina C Tam ◽  
Camillia K Lui ◽  
Katherine J Karriker-Jaffe
Keyword(s):  
Synergistic Effects ◽  
Population Sample ◽  
Heavy Drinking ◽  
Heavy Episodic Drinking ◽  
Interactive Effects ◽  
California Health Interview Survey ◽  
Protective Effects ◽  
Foreign Born ◽  
Ethnic Density ◽  
Nativity Status

Abstract Aims Greater neighborhood co-ethnic density (living in proximity with people sharing an ethnicity) and being foreign-born each can protect against risky drinking, but little is known about whether these two factors interact. Using a representative sample of Latinos and Asians from California, USA, we investigate main and interactive effects of neighborhood co-ethnic density and nativity status in relation to heavy episodic drinking (HED). Methods This study uses the California Health Interview Survey (N = 30,203) linked with neighborhood data to investigate associations of co-ethnic density and nativity status with HED. Co-ethnic density was based on matching each respondent’s ethnicity to the proportion of residents of the corresponding group in their Census tract. Using weighted logistic regression, we first examined main effects of neighborhood co-ethnic density and respondent nativity status on HED. Next, we assessed the interaction of co-ethnic density and nativity status. Finally, we estimated nativity-stratified models to investigate variation in effects of co-ethnic density. Results Co-ethnic density was not associated with HED for the full sample, but US-born nativity status was associated with increased odds of past-year HED. The interaction model showed co-ethnic density and nativity had synergistic effects, whereby greater levels of neighborhood co-ethnic density buffered risk associated with being US-born. Further, greater neighborhood co-ethnic density was associated with reduced odds of HED for US-born respondents, but it was not associated with HED for foreign-born respondents. Conclusions Protective effects of high neighborhood co-ethnic density on HED are stronger for US-born than for foreign-born Latinos and Asians in California.

Intrahippocampal co-administration of nicotine and O-acetyl-L-carnitine prevents the H-89-induced spatial learning deficits in Morris water maze

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Mahmoud Hashemzaei ◽  
Najmeh Baratzadeh ◽  
Iraj Sharamian ◽  
Sahar Fanoudi ◽  
Mehdi Sanati ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Spatial Memory ◽  
Morris Water Maze ◽  
Spatial Learning ◽  
Water Maze ◽  
Synergistic Effects ◽  
Deionized Water ◽  
Learning Deficits ◽  
Learning Impairments ◽  
Morris Water Maze Task

Abstract Objectives H-89 (a protein kinase AII [PKA II] inhibitor) impairs the spatial memory in the Morris water maze task in rats. In the present study, we aimed to study the protective effects of nicotine and O-acetyl-L-carnitine against H-89-induced spatial memory deficits. Methods Spatial memory impairment was induced by the bilateral intrahippocampal administration of 10 µM H-89 (dissolved in dimethyl sulfoxide, DMSO) to rats. The rats then received bilateral administrations of either nicotine (1 μg/μL, dissolved in saline) or O-acetyl-L-carnitine (100 μM/side, dissolved in deionized water) alone and in combination. Control groups received either saline, deionized water, or DMSO. Results The H-89-treated animals showed significant increases in the time and distance travelled to find hidden platforms, and there was also a significant decrease in the time spent in the target quadrant compared to DMSO-treated animals. Nicotine and O-acetyl-L-carnitine had no significant effects on H-89-induced spatial learning impairments alone, but the bilateral intrahippocampal co-administration of nicotine and O-acetyl-L-carnitine prevented H-89-induced spatial learning deficits and increased the time spent in the target quadrant in comparison with H-89-treated animals. Conclusions Our results indicated the potential synergistic effects of nicotine and O-acetyl-L-carnitine in preventing protein kinase AII inhibitor (H-89)-induced spatial learning impairments.

scholarly journals Combined secondary compounds naturally found in nectars enhance honeybee cognition and survival

2021 ◽  
Vol 224 (6) ◽  
Author(s):  
Ignacio L. Marchi ◽  
Florencia Palottini ◽  
Walter M. Farina
Keyword(s):  
Cognitive Ability ◽  
Sucrose Solution ◽  
Synergistic Effects ◽  
Secondary Compounds ◽  
Learning Performance ◽  
Memory Retention ◽  
Olfactory Conditioning ◽  
Significant Survival ◽  
Short And Long Term

ABSTRACT The alkaloid caffeine and the amino acid arginine are present as secondary compounds in nectars of some flower species visited by pollinators. Each of these compounds affects honeybee appetitive behaviours by improving foraging activity and learning. While caffeine potentiates responses of mushroom body neurons involved in honeybee learning processes, arginine acts as precursor of nitric oxide, enhancing the protein synthesis involved in memory formation. Despite existing evidence on how these compounds affect honeybee cognitive ability individually, their combined effect on this is still unknown. We evaluated acquisition and memory retention in a classical olfactory conditioning procedure, in which the reward (sucrose solution) contained traces of caffeine, arginine or a mixture of the two. The results indicate that the presence of the single compounds and their most concentrated mixture increases bees' learning performance. However, memory retention, measured in the short and long term, increases significantly only in those treatments offering combinations of the two compounds in the reward. Additionally, the most concentrated mixture triggers a significant survival rate in the conditioned bees. Thus, some nectar compounds, when combined, show synergistic effects on cognitive ability and survival in an insect.

scholarly journals Protective Effects of Glutamine and Leucine Supplementation on Sepsis-Induced Skeletal Muscle Injuries

2021 ◽  
Vol 22 (23) ◽  
pp. 13003
Author(s):  
Yu-Chen Hou ◽  
Man-Hui Pai ◽  
Jin-Ming Wu ◽  
Po-Jen Yang ◽  
Po-Chu Lee ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Synergistic Effects ◽  
Hypoxia Inducible Factor ◽  
Cecal Ligation ◽  
Protective Effects ◽  
Muscle Injuries ◽  
Leucine Supplementation ◽  
Inflammatory Monocytes ◽  
Inflammatory Phenotype ◽  
Anti Inflammatory

This study investigated the effects of l-glutamine (Gln) and/or l-leucine (Leu) administration on sepsis-induced skeletal muscle injuries. C57BL/6J mice were subjected to cecal ligation and puncture to induce polymicrobial sepsis and then given an intraperitoneal injection of Gln, Leu, or Gln plus Leu beginning at 1 h after the operation with re-injections every 24 h. All mice were sacrificed on either day 1 or day 4 after the operation. Blood and muscles were collected for analysis of inflammation and oxidative damage-related biomolecules. Results indicated that both Gln and Leu supplementation alleviated sepsis-induced skeletal muscle damage by reducing monocyte infiltration, calpain activity, and mRNA expression levels of inflammatory cytokines and hypoxia-inducible factor-1α. Furthermore, septic mice treated with Gln had higher percentages of blood anti-inflammatory monocytes and muscle M2 macrophages, whereas Leu treatment enhanced the muscle expressions of mitochondrion-related genes. However, there were no synergistic effects when Gln and Leu were simultaneously administered. These findings suggest that both Gln and Leu had prominent abilities to attenuate inflammation and degradation of skeletal muscles in the early and/or late phases of sepsis. Moreover, Gln promoted the switch of leukocytes toward an anti-inflammatory phenotype, while Leu treatment maintained muscle bioenergetic function.

Zinc Chloride and Lead Acetate-Induced Passive Avoidance Memory Retention Deficits Reversed by Nicotine and Bucladesine in Mice

2015 ◽  
Vol 169 (1) ◽  
pp. 106-113 ◽  
Author(s):  
Kaveh Tabrizian ◽  
Abdolmajid Yazdani ◽  
Behnam Baheri ◽  
Borna Payandemehr ◽  
Mehdi Sanati ◽  
...  
Keyword(s):  
Passive Avoidance ◽  
Zinc Chloride ◽  
Lead Acetate ◽  
Memory Retention ◽  
Avoidance Memory

scholarly journals Apolipoprotein E Antibodies Affect the Retention of Passive Avoidance Memory in the Chick

1998 ◽  
Vol 6 (3) ◽  
pp. 29-40 ◽  
Author(s):  
Chris Lancashire ◽  
Radmila Mileusnic ◽  
Steven P.R. Rose
Keyword(s):  
Risk Factors ◽  
Apolipoprotein E ◽  
Passive Avoidance ◽  
Residence Time ◽  
Memory Formation ◽  
Avoidance Task ◽  
Brain Distribution ◽  
The Brain ◽  
Avoidance Memory

Isoforms of apolipoprotein E (ApoE) have been implicated as risk factors in Alzheimer’s disease. We have, therefore, examined the possible role of ApoE in memory formation, using a one-trial passive avoidance task in day-old chicks. Birds were trained on the task and then at various times pre or post-training were injected intracerebrally with anti-ApoE. Immunofluorescence staining demonstrated the presence of the antibody bound to the neuropil, close to the injection site and adjacent to the ventricle, with a residence time in the brain of up to 30 min. Chicks that were injected 30 min pre-training or just post-training with 5μg/ hemisphere of the antibody learned the task, but were amnesic when tested at 30 min or at subsequent times up to 24 hr Post-training. When tested at 24 hr, birds injected 5.5 hr post-training showed unimpaired retention. Birds injected with 5μg/hemisphere of anti-ApoA-I (which has a brain distribution similar to that of anti-ApoE) at 30 min pretraining showed no amnesia, indicating the specificity of the effect to the ApoE. Possible mechanisms for this effect are discussed.

scholarly journals L-Carnosine Stimulation of Coenzyme Q10 Biosynthesis Promotes Improved Mitochondrial Function and Decreases Hepatic Steatosis in Diabetic Conditions

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 793
Author(s):  
Cheng Schwank-Xu ◽  
Elisabete Forsberg ◽  
Magnus Bentinger ◽  
Allan Zhao ◽  
Ishrath Ansurudeen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Mouse Model ◽  
Mitochondrial Function ◽  
Diabetes Complications ◽  
Synergistic Effects ◽  
Coenzyme Q ◽  
Protective Effects ◽  
Beneficial Effects

Mitochondrial dysfunction in type 2 diabetes leads to oxidative stress, which drives disease progression and diabetes complications. L-carnosine, an endogenous dipeptide, improves metabolic control, wound healing and kidney function in animal models of type 2 diabetes. Coenzyme Q (CoQ), a component of the mitochondrial electron transport chain, possesses similar protective effects on diabetes complications. We aimed to study the effect of carnosine on CoQ, and assess any synergistic effects of carnosine and CoQ on improved mitochondrial function in a mouse model of type 2 diabetes. Carnosine enhanced CoQ gene expression and increased hepatic CoQ biosynthesis in db/db mice, a type 2 diabetes model. Co-administration of Carnosine and CoQ improved mitochondrial function, lowered ROS formation and reduced signs of oxidative stress. Our work suggests that carnosine exerts beneficial effects on hepatic CoQ synthesis and when combined with CoQ, improves mitochondrial function and cellular redox balance in the liver of diabetic mice. (4) Conclusions: L-carnosine has beneficial effects on oxidative stress both alone and in combination with CoQ on hepatic mitochondrial function in an obese type 2 diabetes mouse model.

Ameliorative Effect of Natural and Synthetic Antioxidants on Arsenic Toxicity in Male Mice: Biochemical and Histological Perspectives

2018 ◽  
Author(s):  
Sayed Amer ◽  
Yousif Al-Zahrani ◽  
Mohammad AL-Harbi
Keyword(s):  
Mononuclear Cell ◽  
Lethal Dose ◽  
Treated Group ◽  
Blood Parameters ◽  
Protective Role ◽  
Cell Infiltration ◽  
Arsenic Toxicity ◽  
Protective Effects ◽  
Mononuclear Cell Infiltration ◽  
Sodium Arsenate

The present study aimed to investigate the protective effects of some natural and artificial antioxidants on the hepato-renal injuries induced by arsenic toxicity. Sixty adult male albino mice weighing 30-40 g were subjected to a sub-lethal dose of sodium arsenate (40 mg/kg body weight) to investigate hematological, biochemical and histopathological alterations resulting from arsenic-induced hepato-renal toxicity. Arsenic-exposed mice were also co-treated with different antioxidants including green tea, garlic and vitamin C to reveal their potential protective role. The antioxidants induced normalization of all blood parameters that showed significant declines by arsenic toxicity. ALT and AST activities were significantly increased in sodium arsenate treated group compared to all other groups. These enzymes did not acquire insignificant differences in antioxidants-treated groups compared to the control mice. Creatinine and urea were significantly increased in arsenate treated mice and become normal in mice co-treated with different antioxidants. Liver sections of arsenate treated mice showed venous congestion, sinusoidal dilatation, mononuclear cell infiltration and periportal fibrosis. Renal sections in the same groups revealed interstitial hemorrhages, mononuclear cell infiltration, glomerulonephritis and proximal tubular necrosis. Hepato-renal histopathology was greatly reduced, particularly, in groups received combined antioxidants. The used antioxidants, therefore, exhibited potential protection against hepato-renal induced arsenic toxicity.

Echinacoside ameliorates the memory impairment and cholinergic deficit induced by amyloid beta peptides via the inhibition of amyloid deposition and toxicology

2017 ◽  
Vol 8 (6) ◽  
pp. 2283-2294 ◽  
Author(s):  
Young-Ji Shiao ◽  
Muh-Hwan Su ◽  
Hang-Ching Lin ◽  
Chi-Rei Wu
Keyword(s):  
Amyloid Beta ◽  
Memory Impairment ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Protective Effects ◽  
Neuronal Function ◽  
Amyloid Beta Peptides ◽  
Beta Peptides ◽  
Amyloid Cascade

This study investigates the role of the amyloid cascade and central neuronal function on the protective effects of echinacoside in amyloid β peptide 1-42 (Aβ 1-42)-treated SH-SY5Y cells and an Aβ 1-42-infused rat.

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