Can Social Instability, Food Deprivation and Food Inequality Accelerate Neuronal Aging?

Based on both animal and human studies, inequality in food intake and social instability has adverse effects on the health of individuals and the community. However, it is not known whether social instability, food deprivation and food inequality affect neuronal death and premature aging in young animals. To address this question, the effects of these adverse situations, histopathological changes in hippocampal pyramidal cells and aging process were investigated.Forty eight New Zeeland white male rabbits were divided into six groups and all of them were housed in similar conditions, with 2 animals per cage in a temperature-controlled colony room under light–dark cycle . All experimental animals were fed on standard rabbit commercial pellets and different social situations such as food deprivation, inequality in food intake, and unstable social status were applied to experimental groups during eight weeks. Afterward, lipofuscin accumulation and apoptosis, as main markers of aging, were compared to the control group by Long Ziehl Nelseen staining and the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL reaction) assay to reveal the rate of lipofuscin pigment accumulation and TUNEL-reactive apoptotic bodies in the hippocampal pyramidal cells. Serum cortisol level was also measured. Inequality in social situation raised chronic stress (i.e. food deprivation, social inequality and instability) and caused significant changes in lipofuscin accumulation in hippocampal pyramidal cells in comparison to the control group (p<0.005) . The results also showed a significant increase in the ratio of apoptotic to normal cells in all of the stressed groups compared to the control group (p<0.05). Moreover, application of the social inequality and stresses alone or together modulated levels of cortisol in the experimental group. These findings suggest that food deprivation, inequality and social instability enhance the susceptibility of hippocampal pyramidal cells to apoptosis and premature aging induced by lipofuscin accumulation.Forty eight New Zeeland white male rabbits were divided into six groups and all of them were housed in similar conditions, with 2 animals per cage in a temperature-controlled colony room under light–dark cycle. All experimental animals were fed on standard rabbit commercial pellets and different social situations such as food deprivation, inequality in food intake, and unstable social status were applied to experimental groups during eight weeks. Afterward, lipofuscin accumulation and apoptosis, as main markers of aging, were compared to the control group by Long Ziehl Nelseen staining and the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL reaction) assay to reveal the rate of lipofuscin pigment accumulation and TUNEL-reactive apoptotic bodies in the hippocampal pyramidal cells. Serum cortisol level was also measured. Inequality in social situation raised chronic stress (i.e. food deprivation, social inequality

Unstable social situation and food inequality can promote accumulation of lipofuscin and induced apoptosis in hepatocytes

Introduction: Based on both animal and human studies, inequality and social injustice haveadverse effects on individual and community health. However, it is not yet known whether socialinstability and food inequality can cause the premature aging hepatocytes death in young people. Toaddress this question, the effects of food intake inequality with or without unstable social statuswere evaluated and histopathological changes in hepatocytes and aging process investigated as well.Material and Methods: Forty eight Newzeland white male rabbits were divided into six groups anddifferent social situations were applied to some groups during eight weeks. After the end of theperiod of the experiment, lipofuscin accumulation and apoptosis as two main markers of agingwere studied by long Zeihl Nelseen staining and the terminal deoxynucleotidyl transferase dUTPnike end labeling (TUNEL reaction) of the hepatocytes respectively. Serum cortisol level was alsomeasured.Results: The simultaneous application of the mentioned situations (i.e. food restriction, socialinequality and changed cage-mate), caused significant change in lipofuscin accumulation in thehepatocytes in comparison with the control group (p<0.001). In addition, application of instability andisolation environment produced significant changes in hepatocytes apoptosis (p<0.05).Conclusion: Accumulation of two main markers of aging increased in hepatocytes and wasaccelerated in the groups with unstable social status

Formation of embryoid bodies from mouse embryonic stem cells cultured on silicon-coated surfaces

Embryoid bodies (EBs) are primitive embryonic structures derived from differentiating embryonic stem cells (ESCs). Many techniques have been used to obtain EBs. Improving the technique of EB formation can help in achieving better results in ESCs differentiation into neurons, myocardiocytes, haemopoeitic cells, and others. We evaluated the use of Sigmacote™ as a hydrophobic substrate to improve EB formation. CCE and P19 cell lines were used to obtain EBs and retinoic acid was used to induce neural differentiation. The results revealed that Sigmacote™, as a hydrophobic substrate, can improve EB formation from ESCs. Our results demonstrate that the silicon-coating of glass petri dishes by Sigmacote™ is an easy and reproducible technique to enhance EB formation from murine ESCs and EC cells