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EN
Background: Different pathological affections of the small intestine cause corresponding morphological and functional changes. The present study was aimed to assess intestinal trehalase activities during ischemia and following reperfusion, correlate them with the pathological changes and determine whether trehalase could be used as a biochemical marker of the intestinal ischemia, ischemia - reperfusion injury. Material and methods: Wistar rats, randomly divided into 5 experimental groups (IR) (each n=15), were subjected to one hour mesenteric ischemia followed by 0, 1, 4, 12 and 24 hours of reperfusion. As a control group sham operated animals were used (n=15). The activity of trehalase was determined using an adapted Dahlqwist method. The range of intestinal injury was determined using histological (histopathological injury index and goblet cell quantification) and immunohistochemical (Ki67, InSitu TUNEL) methods. Results: The highest activities of trehalase were recorded in the control group (C=4.42±0.373 μmol/mg/h). The most altered intestinal histology detected in group IR1 was accompanied by the lowest trehalase activity (IR1=0.97±0.209 μmol/mg/h; p < 0.001 C vs. IR1). Improved histological structure in the remaining reperfusion periods correlated with increase in trehalase activity. Almost normal mucosal histological architecture and 72% of the enzymatic activity were restored after 24 hours of reperfusion (IR24=3.20±0.266 μmol/mg/h; p < 0.01 IR1 vs. IR24). Conclusion: The correlation between intestinal histology and trehalase activities during intestinal injury has been shown. Trehalase activity is closely associated with the status of the histological architecture of the small intestine.
EN
The exposure of gastric mucosa to damaging factors,such as ethanol,water restraint stress,or ischemia followed by reperfusion,produces pathological changes: inflammatory process,hemorrhagic erosions,even acute ulcers.The base of these changes is a disturbance of protective mechanisms and disrupture of gastric mucosal barrier.Previous studies pointed out the role of disturbances of gastric blood flow,mucus secretion and involvement of prostaglandins and nitric oxide formation in the pathomechanism of gastric mucosa lesions.The role of reactive oxygen species (ROS)in these processes has been little studied.Aim:The purpose of our present investigations is to explain the participation of ROS in acute gastric mucosal damage by various irritants.Material and methods:Experiments were carrying out on 80 male Wistar rats.To assess gastric blood flow (GBF)laser Doppler flowmeter was used.The area of gastric lesions was established by planimetry.The levels of proinflammatory cytokines were measured by ELISA technique.The colorimetric assays were used to determine of malondialdehyde (MDA)and 4-hydroxynonenal (4-HNE)as well as superoxide dismutase (SOD)activity.Results:We demonstrated that 3.5 h of water immersion and restraint stress (WRS),30 min of gastric ischemia followed by 60 min of reperfusion or intragastric administration of 100%ethanol,all resulted in appearance of acute gastric mucosal lesions accompanied by a significant decrease of gastric blood flow. These lesions are also accompanied by the significant increase of proinflammatory cytokines including interleukin –1 beta (IL-1 ß )and tumor necrosis factor alpha (TNF alpha )plasma level. Biological effects of ROS were estimated by measuring tissue level of MDA and 4-HNE, the products of lipid peroxydation by ROS,as well as the activity of SOD,the scavanger of ROS.It was established that 3.5 h of WRS,ischemia-reperfusion and 100%ethanol lead to significant increase of MDA and 4-HNE mucosal level,accompanied by a decrease of SOD activity (significant in WRS and ethanol application).Conclusions:The pathogenesis of experimental mucosal damage in rat stomach includes the generation of ROS that seem to play an important role,namely due to generation of lipid peroxides,accompanied by impairment of antioxidative enzyme activity of cells.
12
Content available remote Vasopressin in vascular regulation and water homeostasis in the brain
51%
EN
A specific temporal order of events at the cellular and molecular level occurs in response to injury to the brain. Injury-compromised neurons degenerate while surviving neurons undergo neuritogenesis and synaptogenesis to establish neuronal connectivity destroyed in the injury. Several genes, such as those coding cytoskeletal proteins and growth factors, have been shown to be regulated by AP-1 and NF-kB transcription factors, two of the most studied DNA binding regulatory proteins. Our laboratory has discovered that Fos-related antigen-2 from AP-1 transcription factor family and NF-kB p65 and p50 subunits are induced long-term (days to months) in the brain after neurotoxic, excitotoxic or ischemic insult. Fos-related antigen-2 is induced in neurons in several models of injury and its elevated expression lasts days to months, corresponding to the severity. The time-course of FRA-2 induction is abbreviated with less severe insult (terminal damage) relative to the cell death, but the induction occurs during the period of regeneration and repair in both models. NF-kB p65 is basally expressed in hippocampal and cortical neurons, but is elevated in reactive astrocytes in hippocampus and entorhinal cortex starting at two days and lasting at least two weeks after kainate treatment. Neurons of the hippocampus surviving ischemic or neurotoxic injury increase expression of NF-kB p50 for at least a week after injury, suggesting a function for p50 in neuronal survival and/or repair. The extended expression of these transcription factors implies a role in the activation of genes related to repair and regeneration, such as growth factors and synaptic proteins, after injury to the CNS.
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