Background: Traumatic brain injury is one of the most serious problems of modern medicine that plays the dominant role in the morbidity and mortality of population of the economically developed countries. This article presents the findings of the experimental study of the effect of a mild traumatic brain injury (TBI) on the morphology of rats' kidney. Material and methods: The experiment was performed on 70 adult white rats 3 months of age. The mild TBI was modeled by the Impact-Acceleration Model-free fall of weight in the parieto-occipital area. For histopathological comparison, the samples were taken on the 1st, 3rd, 5th, 7th, 14th, 21st days after TBI. Results: Examination of the rat's kidney histological slides on the 1st, 3rd, 5th, 7th, 14th, and 21st days after the traumatic brain injury showed manifested changes in the bloodstream and structural changes in the kidney parenchyma, particularly, dilatation of the capillaries and veins in the initial period. It also showed perivascular lymphocytic infiltration, dystrophic and necrotic processes in the form of the focal destruction of the renal tubule, and renal corpuscles with diapedesis and perivascular hemorrhages on the 5th and 7th days after the TBI. There were also the focal signs of perivascular and glomerular sclerosis observed on the 14th and 21st days after the injury. Conclusions: The greatest changes in the rats' kidneys appear on the 5th-7th days after the injury, which have a clear tendency to decrease after that.
Traumatic brain injury (TBI) is one of the most severe problems of modern medicine that plays a dominant role in morbidity and mortality in economically developed countries. Our experimental study aimed to evaluate the histological and morphological changes occurring in the liver of adult and juvenile mildly traumatized rats (mTBI) in a time-dependent model. The experiment was performed on 70 adult white rats at three months of age and 70 juvenile rats aged 20 days. The mTBI was modelled by the Impact-Acceleration Model-free fall of weight in the parieto-occipital area. For histopathological comparison, the samples were taken on the 1st, 3rd, 5th, 7th, 14th, and 21st days after TBI. In adult rats, dominated changes in the microcirculatory bed in the form of blood stasis in sinusoidal capillaries and veins, RBC sludge, and adherence to the vessel wall with the subsequent appearance of perivascular and focal leukocytic infiltrates. In juvenile rats, changes in the parenchyma in the form of hepatocyte dystrophy prevailed. In both groups, the highest manifestation of the changes was observed on 5–7 days of the study. On 14–21 days, compensatory phenomena prevailed in both groups. Mild TBI causes changes in the liver of both adult and juvenile rats. The morphological pattern and dynamics of liver changes, due to mild TBI, are different in adult and juvenile rats.
The immunoproteasome is a central protease complex required for optimal antigen presentation. Immunoproteasome activity is also associated with facilitating degradation of misfolded and oxidized proteins, which prevents cellular stress. While extensively studied during diseases with increasing evidence suggesting a role for the immunoproteasome during pathological conditions including neurodegenerative diseases, this enzyme complex is believed to be mainly inactive in the healthy brain. Here, we show an age-dependent increase in polyubiquitination in the brain of wild-type mice, accompanied with induction of immunoproteasomes, which was most prominent in neurons and microglia. In contrast, mice completely lacking immunoproteasomes (triple-knockout (TKO) mice deficient for LMP2, LMP7 and MECL-1), displayed a strong increase in polyubiquitinated proteins already in the young brain and developed spontaneous epileptic seizures, beginning at the age of 6 months. Injections of kainic acid led to high epilepsy-related mortality of aged TKO mice, confirming increased pathological hyperexcitability states. Notably, the expression of the immunoproteasome was reduced in the brains of patients suffering from epilepsy. In addition, aged TKO mice showed increased anxiety, tau hyperphosphorylation and degeneration of Purkinje cell population with the resulting ataxic symptoms and locomotion alterations. Collectively, our study suggests a critical role for the immunoproteasome in the maintenance of a healthy brain during aging.
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