Neuroinflammatory Cytokine Response, Neuronal Death, and Microglial Proliferation in the Hippocampus of Rats During the Early Period After Lateral Fluid Percussion-Induced Traumatic Injury of the Neocortex

Abstract

Time course of changes in neuroin ammatory processes in the dorsal and ventral hippocampus was studied during the early period after lateral uid-percussion-induced neocortical traumatic brain injury (TBI) in the ipsilateral and contralateral hemispheres. In the ipsilateral hippocampus, neuroin ammation (increase in expression of pro-in ammatory cytokines) was evident from day 1 after TBI and ceased by day 14, while in the contralateral hippocampus it was mainly limited to the dorsal part on day 1. TBI induced an increase in hippocampal corticosterone level on day 3 bilaterally and an accumulation of Il1b on day 1 in the ipsilateral hippocampus. Activation of microglia was observed from day 7 in different hippocampal areas of both hemispheres. Neuronal cell loss was detected in the ipsilateral dentate gyrus on day 3 and extended to the contralateral hippocampus by day 7 after TBI. The data suggest that TBI results in distant hippocampal damage (delayed neurodegeneration in the dentate gyrus and microglia proliferation in both the ipsilateral and contralateral hippocampus), the time course of this damage being different from that of the neuroin ammatory response.

Cannabidiol inhibits neuroinflammatory responses and circuit-associated synaptic loss following damage to a songbird vocal pre-motor cortical-like region

“…( E ) Expression of the marker of oxidative stress, superoxide dismutase 2 (SOD2) was decreased within HVC and RA. Note that tissue was obtained 24 h post-lesion and thus represents a “snap-shot” of inflammatory cytokine expression that is known to vary with time post-injury 24 . Group differences were assessed by mixed-models ANOVA with Sidak’s multiple comparison correction.…”

A Panax quinquefolius-Based Preparation Prevents the Impact of 5-FU on Activity/Exploration Behaviors and Not on Cognitive Functions Mitigating Gut Microbiota and Inflammation in Mice

“…In addition, studies showing that i.p. LPS or traumatic brain injury induces acute and/or sustained cytokines mRNA expression in the dHp and vHp, respectively [ 86 , 87 ], suggest that the dHp develops this neuroinflammation first and transiently, which then spreads to the vHp over a longer time. While 5-FU administration drastically altered neurogenesis in the dHp and VHp, Qiseng ® , and potentially its components, such as ginsenosides or P. qfolius metabolites, would be more specific to the neuroinflammatory pathway recruited in the vHp.…”

Neuroinflammation as secondary damage in head injury

“…Продукты распада элементов крови в субарахноидальном пространстве приводят к развитию хронического асептического лептоменингита и спаечного процесса. Белок пероксиредоксин, который в большом количестве содержится в эритроцитах, запускает дальнейший каскад воспалительных реакций и апоптоз нейронов при помощи NF-κB, что способствует дальнейшему развитию воспаления и гидроцефалии [17,[32][33][34][35][36][37].…”

“…Вначале микроглия фенотипа М1 защищает оставшиеся нейроны от дальнейшего разрушения, однако чрезмерная активация нарушает такие процессы, как олигодендрогенез, созревание олигодендроцитов и их выживаемость за счёт секреции ФНО-α, увеличивает нейротоксичность из-за секретируемых провоспалительных факторов, что в дальнейшем запускает процессы нейродегенерации, опосредованные микроглией. M2-микроглия секретирует противовоспалительные цитокины ИЛ-4, ИЛ-13, которые, как предполагают, уменьшают воспаление и улучшают восстановление тканей [10,11,[17][18][19][20]. Однако активация микроглии по типу M2, в отличие от М1, носит кратковременный характер.…”