Stress, encompassing psychological, physical, and physiological challenges, is an important factor affecting an individual's well-being and potentially leading to psychiatric, neurodegenerative, immune, and metabo...
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Stress, encompassing psychological, physical, and physiological challenges, is an important factor affecting an individual's well-being and potentially leading to psychiatric, neurodegenerative, immune, and metabolic disorders. However, not everyone exposed to stress develops these conditions, highlighting the concept of resilience. Resilience is a dynamic process categorized into four dimensions: pre-existing resilience capacity, ongoing resilience processes, post-stress resilience outcomes, and recovery from psychopathologies. These dimensions involve genomic, cellular, and systemic interactions influenced by genetic factors, early life experiences, adult life experiences in addition to community/environmental factors, and health behaviors. The biological response to stress encompasses endocrine, autonomic, immunological, and behavioral components, modulated by stressor characteristics and individual traits. Due to the limitations in studying stress and resilience in humans, translational models using rodents and cell cultures are essential. Rodent models include acute, chronic, and traumatic stress paradigms, aiding the study of stress-related behavioral and molecular outcomes. Additionally, early life stress models, such as prenatal stress and maternal separation, provide insights into developmental impacts. In this review, first, rodent models for lifelong stress exposure will be summarized considering their validity, advantages, and limitations. Subsequently, an overview of models designed to enhance resilience capacity and process in rodents, and later the behavioral models employed to study the outcomes of resilience will be given. Lastly, the focus will be shifted to cell culture and iPSCs models. Finally, future considerations focused on improving translational models used to study stress and resilience will be discussed. It is aimed to provide an overview of designs for translational stress and resilience models to access more effective translational biom
Cytokines and chemokines play important roles in inflammation and repair following brain injury. M1 microglia are pro-inflammatory which produce cytokines and lead to neural injury;in contrast, M2 microglia are anti-i...
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Cytokines and chemokines play important roles in inflammation and repair following brain injury. M1 microglia are pro-inflammatory which produce cytokines and lead to neural injury;in contrast, M2 microglia are anti-inflammatory, release neurotrophic factors, and promote neural repair processes. Chemokine CCL5, increased after TBI, shows a neuroprotective function by reducing oxidative stress. CCL5 may contribute to the balance between oxidative stress and immune responses after brain injury. Herein, we investigated the role of CCL5 in microglial polarization after mild traumatic brain injury, focusing on the cerebral cortex.C57BL/6 and CCL5 knockout (CCL5-KO) mice were given a mild traumatic brain injury (TBI) using weight-drop. Neurological parameters such as motor and sensory functions were analyzed by mNSS score, accelerating rotarod, beam walking, and adhesive removal tests. Oxidative stress and neuron damage were measured by NADPH oxidase activity, hypoxyloprobe staining and FJC. Performance of motor and sensory functions in both WT and CCL5-KO mice were impaired after brain injury which recovered after 7 days-post-injury (dpi) in the WT group but only after 14 days in the CCL5-KO mouse group. RT-qPCR analysis revealed that pro-inflammation cytokines - IL-1β, TNF-α, and IL-6 were higher in CCL5-KO mice compared to WT mice at 4 and 14 dpi. In contrast, M2-like microglia markers - IL-10 and Agr-1 were increased in WT mouse cortical tissue at 4 dpi. Oxidative stress increased both M1 and M2- related cytokine expression in BV2 cells treated with H 2 O 2;CCL5 treatment increased M2- but suppressed M1- related cytokine gene activation. Intranasal delivery of CCL5 reduced neuronal oxidative stress, increased IL-10 expression and improved motor and sensory functions in CCL5-KO mice after brain *** summary, CCL5, which alters immune responses and protects neurons from TBI damage, has an important function in regulating M2-like microglial polarization during post-
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