scholarly journals Empathy in stroke rats is modulated by social settings

2019 ◽  
Vol 40 (6) ◽  
pp. 1182-1192 ◽  
Author(s):  
Kazutaka Shinozuka ◽  
Naoki Tajiri ◽  
Hiroto Ishikawa ◽  
Julian P Tuazon ◽  
Jea-Young Lee ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Psychological Stress ◽  
Physiological Stress ◽  
Advanced Glycation Endproducts ◽  
Plasma Corticosterone ◽  
Adult Rats ◽  
Glycation Endproducts ◽  
Age Related ◽  
Social Settings ◽  
General Locomotor Activity

Rodents display “empathy” defined as perceived physical pain or psychological stress by cagemates when co-experiencing socially distinct traumatic events. The present study tested the hypothesis that empathy occurs in adult rats subjected to an experimental neurological disorder, by allowing co-experience of stroke with cagemates. Psychological stress was measured by general locomotor activity, Rat Grimace Scale (RGS), and plasma corticosterone. Physiological correlates were measured by Western blot analysis of advanced glycation endproducts (AGE)-related proteins in the thymus. General locomotor activity was impaired in stroke animals and in non-stroke rats housed with stroke rats suggesting transfer of behavioral manifestation of psychological stress from an injured animal to a non-injured animal leading to social inhibition. RGS was higher in stroke rats regardless of social settings. Plasma corticosterone levels at day 3 after stroke were significantly higher in stroke animals housed with stroke rats, but not with non-stroke rats, indicating that empathy upregulated physiological stress level. The expression of five proteins related to AGE in the thymus reflected the observed pattern of general locomotor activity, RGS, and plasma corticosterone levels. These results indicate that stroke-induced psychological stress manifested on both the behavioral and physiological levels and appeared to be affected by empathy-associated social settings.

Pituitary-adrenal response to bacterial endotoxin in developing rats

1988 ◽  
Vol 255 (4) ◽  
pp. E525-E530 ◽  
Author(s):  
L. Witek-Janusek
Keyword(s):  
Plasma Corticosterone ◽  
Neonatal Rat ◽  
Bacterial Endotoxin ◽  
Plasma Acth ◽  
Adult Rats ◽  
Age Related ◽  
Corticosterone Response ◽  
Adrenal Response ◽  
Old Rats ◽  
Related Pattern

The neonatal rat is very sensitive to the lethal effects of bacterial endotoxin. Because of the adaptive importance of pituitary-adrenal secretions to stress, this study examined the ontogeny of the plasma corticosterone and adrenocorticotropic hormone (ACTH) responses to endotoxin. The lethal sensitivity of young rats to endotoxin ranged from 0.5 to 30 mg/kg (ip) in the 1- to 21-day-old rat. After endotoxin treatment, the 1- and 2-day-old rat showed marked elevations of corticosterone similar in magnitude to that seen in 21-day-old and adult rats; however, significantly depressed corticosterone increments were observed in the 5-, 10-, and 14-day-old rats. This age-related pattern of adrenocortical secretion was correlated with the developing rat's corticosterone response to exogenous ACTH. In contrast, endotoxin administered to 5-, 10-, and 14-day-old rats resulted in increments of plasma ACTH similar to those observed in the 21-day-old and adult rats. Although plasma ACTH levels increased by 84-127% in the 1- and 2-day-old rats, these increases were significantly less than those of rats at all other ages tested. Thus the newborn rat mounts an effective corticosterone response to endotoxin, loses this ability between ages 5-14 days, and regains this response at 21 days of age. Because the hyporesponsive ages exhibit a marked increase in ACTH secretion, the loss of the adrenocortical response to endotoxin appears to be a result of a depressed responsiveness of the adrenal cortex to ACTH.

scholarly journals Metaflammation: Tissue-Specific Alterations of the NLRP3 Inflammasome Platform in Metabolic Syndrome

2018 ◽  
Vol 25 (11) ◽  
pp. 1294-1310 ◽  
Author(s):  
Raffaella Mastrocola ◽  
Manuela Aragno ◽  
Giuseppe Alloatti ◽  
Massimo Collino ◽  
Claudia Penna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Advanced Glycation Endproducts ◽  
Low Grade ◽  
Advanced Glycation ◽  
Added Sugars ◽  
Physiological Ageing ◽  
Glycation Endproducts ◽  
Inflammatory Status ◽  
Age Related

In the last decades, the extension of life expectancy and the increased consumption of foods rich in saturated fats and added sugars have exposed the general population to emerging health problems. The prevalence of metabolic syndrome (MS), composed of a cluster of factors as obesity, dyslipidemia, hyperglycemia, and hypertension, is rapidly increasing in industrialized and developing countries leading to precocious onset of age-related diseases. Indeed, oxidative stress, accumulation of advanced glycation endproducts, and a chronic low-grade inflammation are common features of MS and physiological ageing. In particular, the entire set of MS factors contributes to the development of an inflammatory status named metaflammation, which has been associated with activation of early innate immune response through the assembling of the multiprotein complex inflammasome. The most investigated family of inflammasome platforms is the NOD-like receptor pyridine containing (NLRP) 3, which is activated by several exogenous and endogenous stimuli, leading to the sequential cleavage of caspase-1 and IL-1β, followed by secretion of active IL-1β. We here collect the most recent findings on NLRP3 activation in MS providing evidence of its central role in disease progression and organ dysfunction in target tissues of metaflammation, in particular in cardiovascular, hepatic and renal complications, with a focus on oxidative stress and advanced glycation endproducts. A wide overview of the most promising strategies for the modulation of NLRP3 activation and related metabolic repercussions is also provided, since the finding of specific pharmacological tools is an urgent requirement to reduce the social and economic burden of MS- and elderly-associated diseases.

The role of methylglyoxal and the glyoxalase system in diabetes and other age-related diseases

2015 ◽  
Vol 128 (12) ◽  
pp. 839-861 ◽  
Author(s):  
Dionne E.M. Maessen ◽  
Coen D.A. Stehouwer ◽  
Casper G. Schalkwijk
Keyword(s):  
Advanced Glycation Endproducts ◽  
Treatment Strategies ◽  
Glyoxalase System ◽  
Dicarbonyl Compound ◽  
Glycation Endproducts ◽  
Age Related ◽  
Key Enzyme ◽  
The Central Nervous System ◽  
New Treatment

The formation and accumulation of advanced glycation endproducts (AGEs) are related to diabetes and other age-related diseases. Methylglyoxal (MGO), a highly reactive dicarbonyl compound, is the major precursor in the formation of AGEs. MGO is mainly formed as a byproduct of glycolysis. Under physiological circumstances, MGO is detoxified by the glyoxalase system into D-lactate, with glyoxalase I (GLO1) as the key enzyme in the anti-glycation defence. New insights indicate that increased levels of MGO and the major MGO-derived AGE, methylglyoxal-derived hydroimidazolone 1 (MG-H1), and dysfunctioning of the glyoxalase system are linked to several age-related health problems, such as diabetes, cardiovascular disease, cancer and disorders of the central nervous system. The present review summarizes the mechanisms through which MGO is formed, its detoxification by the glyoxalase system and its effect on biochemical pathways in relation to the development of age-related diseases. Although several scavengers of MGO have been developed over the years, therapies to treat MGO-associated complications are not yet available for application in clinical practice. Small bioactive inducers of GLO1 can potentially form the basis for new treatment strategies for age-related disorders in which MGO plays a pivotal role.

scholarly journals Polymorphisms in Glyoxalase I Gene Are Not Associated with Glyoxalase I Expression in Whole Blood or Markers of Methylglyoxal Stress: The CODAM Study

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 219
Author(s):  
Kim Maasen ◽  
Nordin M. J. Hanssen ◽  
Carla J. H. van der Kallen ◽  
Coen D. A. Stehouwer ◽  
Marleen M. J. van Greevenbroek ◽  
...  
Keyword(s):  
Multiple Testing ◽  
Advanced Glycation Endproducts ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Glyoxalase I ◽  
Glycation Endproducts ◽  
Fasting Plasma ◽  
Age Related ◽  
Rate Limiting

Glyoxalase 1 (Glo1) is the rate-limiting enzyme in the detoxification of methylglyoxal (MGO) into D-lactate. MGO is a major precursor of advanced glycation endproducts (AGEs), and both are associated with development of age-related diseases. Since genetic variation in GLO1 may alter the expression and/or the activity of Glo1, we examined the association of nine SNPs in GLO1 with Glo1 expression and markers of MGO stress (MGO in fasting plasma and after an oral glucose tolerance test, D-lactate in fasting plasma and urine, and MGO-derived AGEs CEL and MG-H1 in fasting plasma and urine). We used data of the Cohort on Diabetes and Atherosclerosis Maastricht (CODAM, n = 546, 60 ± 7 y, 25% type 2 diabetes). Outcomes were compared across genotypes using linear regression, adjusted for age, sex, and glucose metabolism status. We found that SNP4 (rs13199033) was associated with Glo1 expression (AA as reference, standardized beta AT = −0.29, p = 0.02 and TT = −0.39, p = 0.3). Similarly, SNP13 (rs3799703) was associated with Glo1 expression (GG as reference, standardized beta AG = 0.17, p = 0.14 and AA = 0.36, p = 0.005). After correction for multiple testing these associations were not significant. For the other SNPs, we observed no consistent associations over the different genotypes. Thus, polymorphisms of GLO1 were not associated with Glo1 expression or markers of MGO stress, suggesting that these SNPs are not functional, although activity/expression might be altered in other tissues.

scholarly journals Redox Signaling and Advanced Glycation Endproducts (AGEs) in Diet-Related Diseases

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 142 ◽  
Author(s):  
Vanesa Cepas ◽  
Massimo Collino ◽  
Juan C. Mayo ◽  
Rosa M. Sainz
Keyword(s):  
Oxidative Stress ◽  
Ex Vivo ◽  
Advanced Glycation Endproducts ◽  
Antioxidant Properties ◽  
Protein Glycation ◽  
Ros Production ◽  
Advanced Glycation ◽  
Glycation Endproducts ◽  
Sugar Intake ◽  
Age Related

Diets are currently characterized by elevated sugar intake, mainly due to the increased consumption of processed sweetened foods and drinks during the last 40 years. Diet is the main source of advanced glycation endproducts (AGEs). These are toxic compounds formed during the Maillard reaction, which takes place both in vivo, in tissues and fluids under physiological conditions, favored by sugar intake, and ex vivo during food preparation such as baking, cooking, frying or storage. Protein glycation occurs slowly and continuously through life, driving AGE accumulation in tissues during aging. For this reason, AGEs have been proposed as a risk factor in the pathogenesis of diet-related diseases such as diabetes, insulin resistance, cardiovascular diseases, kidney injury, and age-related and neurodegenerative diseases. AGEs are associated with an increase in oxidative stress since they mediate the production of reactive oxygen species (ROS), increasing the intracellular levels of hydrogen peroxide (H2O2), superoxide (O2−), and nitric oxide (NO). The interaction of AGEs with the receptor for AGEs (RAGE) enhances oxidative stress through ROS production by NADPH oxidases inside the mitochondria. This affects mitochondrial function and ultimately influences cell metabolism under various pathological conditions. This short review will summarize all evidence that relates AGEs and ROS production, their relationship with diet-related diseases, as well as the latest research about the use of natural compounds with antioxidant properties to prevent the harmful effects of AGEs on health.

scholarly journals Antiaging Effect of Pine Pollen in Human Diploid Fibroblasts and in a Mouse Model Induced by D-Galactose

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Gen-Xiang Mao ◽  
Ling-Di Zheng ◽  
Yong-Bao Cao ◽  
Zhuo-Mei Chen ◽  
Yuan-Dong Lv ◽  
...  
Keyword(s):  
Replicative Senescence ◽  
Advanced Glycation Endproducts ◽  
Accelerated Aging ◽  
Inhibitory Effect ◽  
Aging Effects ◽  
Glycation Endproducts ◽  
Human Diploid Fibroblasts ◽  
Age Related ◽  
Pine Pollen

The present paper was designed to investigate the effect of pine pollen against aging in human diploid fibroblast 2BS cells and in an accelerated aging model, which was established by subcutaneous injections with D-galactose daily for 8 weeks in C57BL/6J mice. Pine pollen (1 mg/mL and 2 mg/mL) is proved to delay the replicative senescence of 2BS cells as evidenced by enhanced cell proliferation, decreased SA-β-Gal activity, and reversed expression of senescence-associated molecular markers, such as p53,p21Waf1,p16INK4a, PTEN, andp27Kip1in late PD cells. Besides, pine pollen reversed D-galactose-induced aging effects in neural activity and inflammatory cytokine levels, as indicated by improved memory latency time and reduced error rate in step-down test and decreased concentrations of IL-6 and TNF-α in model mice. Similar to the role of AGEs (advanced glycation endproducts) formation inhibitor aminoguanidine (AG), pine pollen inhibited D-galactose-induced increment of AGEs levels thus reversed the aging phenotypes in model mice. Furthermore, the declined antioxidant activity was obviously reversed upon pine pollen treatment, which may account for its inhibitory effect on nonenzymatic glycation (NEG)in vivo. Our finding presents pine pollen as an attractive agent with potential to retard aging and attenuate age-related diseases in humans.

Higher habitual intake of dietary dicarbonyls is associated with higher corresponding plasma dicarbonyl concentrations and skin autofluorescence: The Maastricht Study

2021 ◽  
Author(s):  
Kim Maasen ◽  
Simone J P M Eussen ◽  
Jean L J M Scheijen ◽  
Carla J H van der Kallen ◽  
Pieter C Dagnelie ◽  
...  
Keyword(s):  
Advanced Glycation Endproducts ◽  
Plasma Concentrations ◽  
Population Based ◽  
Skin Autofluorescence ◽  
Linear Regression Models ◽  
Clinical Trial Registry ◽  
Cross Sectional ◽  
Glycation Endproducts ◽  
Age Related ◽  
Habitual Intake

Abstract Background Dicarbonyls are highly reactive compounds and major precursors of advanced glycation endproducts (AGEs). Both dicarbonyls and AGEs are associated with development of age-related diseases. Dicarbonyls are formed endogenously, but also during food processing. To what extent dicarbonyls from the diet contribute to circulating dicarbonyls and AGEs in tissues is unknown. Objective To examine cross-sectional associations of dietary dicarbonyl intake with plasma dicarbonyl concentrations and skin AGEs. Design In 2566 individuals of the population based Maastricht Study (age: 60±8 yrs, 50% males, 26% type 2 diabetes), we estimated habitual intake of the dicarbonyls methylglyoxal (MGO), glyoxal (GO), and 3-deoxyglucosone (3-DG), by combining Food Frequency Questionnaires with our dietary dicarbonyl database of MGO, GO, and 3-DG concentrations in >200 commonly-consumed food products. Fasting plasma concentrations of MGO, GO, and 3-DG were measured by UPLC-MS/MS. Skin AGEs were measured as skin autofluorescence (SAF), using the AGE-Reader. Associations of dietary dicarbonyl intake with their respective plasma concentrations and SAF (all standardized) were examined using linear regression models, adjusted for age, sex, potential confounders related to cardio-metabolic risk factors and lifestyle. Results Median intake of MGO, GO, and 3-DG was 3.6, 3.5, and 17 mg/day, respectively. Coffee was the main dietary source of MGO, whereas this was bread for GO and 3-DG. In the fully adjusted models, dietary MGO was associated with plasma MGO (β = 0.08, 95%CI [0.02,0.13]) and SAF (β = 0.12 [0.07,0.17]). Dietary GO was associated with plasma GO (β = 0.10 [0.04,0.16]) but not with SAF. 3-DG was not significantly associated with either plasma 3-DG or SAF. Conclusions Higher habitual intake of dietary MGO and GO, but not 3-DG, was associated with higher corresponding plasma concentrations. Higher intake of MGO was also associated with higher SAF. These results suggest dietary absorption of MGO and GO. Biological implications of dietary absorption of MGO and GO need to be determined. Clinical Trial Registry number: The study has been approved by the institutional medical ethical committee (NL31329.068.10) and the Minister of Health, Welfare and Sports of the Netherlands (Permit 131088-105234-PG).

scholarly journals Effects of miniature transponders on physiological stress, locomotor activity, growth and survival in small lizards

2011 ◽  
Vol 32 (2) ◽  
pp. 177-183
Author(s):  
Matthieu Paquet ◽  
Jean-François Le Galliard ◽  
Samuel Perret ◽  
Zorica Pantelic
Keyword(s):  
Locomotor Activity ◽  
Physiological Stress ◽  
Abdominal Cavity ◽  
Plasma Corticosterone ◽  
Negative Effects ◽  
Growth And Survival ◽  
Pit Tags ◽  
Tag Retention ◽  
Common Lizard

AbstractThe marking of small animals for long-term ecological studies requires unambiguous and permanent techniques that cause minimal harm. Toe-clipping is frequently used to identify small lizards in the field, but it has been suggested that passive integrated transponders (PIT tags) should be preferred. Here, we evaluate the costs and benefits of new miniature PIT tags to mark the common lizard (Zootoca vivipara). Our protocol enables permanent marking of lizards as small as 1.3 grams with maximal implantation success in the abdominal cavity. Tag injection caused no observable increase in plasma corticosterone levels over five days and no negative effects on long-term growth and survival. However, tag injection had negative effects on locomotor activity during at least 7 days, possibly implying pain. Continuous research to improve tag implantation is needed because negative effects may be caused by anaesthesia and injection rather the tag retention itself. This study demonstrates the utility of combining physiological, behavioural and life history measurements to assess marking stress and pain in animals.

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