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1

Role of IL-1beta in production of TNF-alpha and IL-6 by peripheral mononuclear cells following subarachnoid hemorrhage in rats

100%
Larysz-Brysz M., Jedrzejowska-Szypulka H., Olakowska E., Lewin-Kowalik J.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Subarachnoid hemorrhage (SAH) develops when extravasated arterial blood enters subarachnoid space and mixes with cerebrospinal fluid. This leads to numerous pathologies, including increased synthesis of proinflammatory cytokines, like interleukin-1β (IL-1β). Through broken blood-brain barrier, IL-1β may stimulate peripheral leukocytes. These peripheral mononuclear cells (PMC) may be an additional source of other cytokines and migrating to the brain they can enhance or reduce the pathologies resulting from SAH. We examined the effect of neutralization of IL-1β on secretion of TNF-α and IL-6 by PMCs in adult rats following SAH. SAH was produced by injection of 150 μL of autologous arterial blood into cisterna magna. In 50% of animals, IL-1β activity was inhibited by intracerebroventricular administration of anti-rat IL-1β antibodies. Control group consisted of sham-operated rats. Ninety minutes or 24 hrs following surgery, blood samples were collected from the extraorbital plexus and centrifuged to separate leukocyte subpopulations. Isolated PMCs (monocytes and lymphocytes) were cultured for 24 hrs and TNF-α and IL-6 concentrations in the supernatants were assessed with ELISA. SAH led to the increase of production of both TNF-α and IL-6 by PMCs. Neutralization of IL-1β activity significantly reduced the concentration of both cytokines 90 min as well as 24 hrs after SAH. The results indicate an important role of IL-1β in the activation of peripheral mononuclear cells in the course of subarachnoid hemorrhage.
2

Serum levels of the S100B protein and neuron - specific enolase are associated with mortality in critically ill patients

100%
Duda I., Krzych L., Jedrzejowska-Szypulka H., Lewin-Kowalik J.
Acta Biochimica Polonica
|
2017
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tom 64
|
nr 4
3

Role of IL-1beta in stimulation of peripheral mononuclear cells to secrete ET-1 and in development of vasospasm following subarachnoid hemorrhage in rats

100%
Jedrzejowska-Szypulka H., Larysz-Borysz M., Woszczycka-Korczynska I., Lewin-Kowalik J.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Subarachnoid hemorrhage (SAH) develops when extravasated arterial blood enters subarachnoid space and mixes with cerebrospinal fluid. As a result, much pathology develops, including arterial vasospasm leading to neuronal ischemia resulting in neurological deficits. Cerebral arteries may be constricted both directly by cytokine influence on arterial smooth muscles and indirectly, through increase of endothelin-1 (ET-1) synthesis or adhesion molecules production. Interleukin-1β (IL-1β) is secreted following SAH and through broken bloodbrain barrier it may lead to the stimulation of peripheral leukocytes. These peripheral mononuclear cells (PMC) may be an additional source of ET-1 and migrating to the brain they can enhance the vasospasm. We examined effect of neutralization of IL-1β on secretion of ET-1 by PMCs as well as on basilar artery vasospasm in rats following SAH. SAH was produced by injection of 150 μL of autologous arterial blood into cisterna magna. In 50% of animals, IL-1β activity was inhibited by intracerebroventricular administration of anti-rat IL-1β antibodies. Control group consisted of sham-operated rats. Ninety minutes or 24 hrs following surgery, blood samples were collected from the extraorbital plexus and centrifuged to separate leukocyte subpopulations. Isolated PMCs (monocytes and lymphocytes) were cultured for 24 hrs and ET-1 concentration in the supernatants was assessed with ELISA. In brain stem specimens, vasospasm was determined. SAH led to the strong vasospasm and increase of production ET-1 by PMCs. Neutralization of IL-1β activity significantly reduced the ET-1 level in both time-points, but led to decrease of vasospasm only after 24 hrs. The results suggest that ET-1 does not influence the vasospasm in the acute phase but is involved in this process 24 hrs after subarachnoid hemorrhage.
4

Solid pituitary adenoma in Eker rats subjected to ketogenic diet

100%
Liskiewicz A., Gendosz D., Jedrzejowska-Szypulka H., Lewin-Kowalik J.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
|
nr Suppl.1
Tuberous sclerosis (TS) is a genetic disease causing non-malignant tumors growth in the brain (e.g. pituitary adenoma) and in other organs. Ketogenic diet is already used in TS patients in treatment of epilepsy. However the mechanism of its influence on tumor growth is still not clear. The Eker rat is a useful model of TS: it has a spontaneous germ line mutation of the TSC2 gene what predisposed them to multiple tumors. In Eker rats, pituitary adenomas are common, occurring in 58% of adults (more than 18-months-old). Methods: Forty six 8-month-old Eker rats (males and females) were used. Twenty six (experimental group) have been maintained on high fat, low carbohydrate ketogenic diet for 6 months, while 20 (control group) received a standard rodent diet. At the age of 14 months rats were sacrificed. Anteroposterior, vertical, and transverse diameters of the found pituitary adenomas were measured. Size of tumors was calculated by using the formula for volume of the ellipsoid. Results: 8% animals from experimental group and 20% from control group have developed pituitary adenomas. Mean tumor volume in experimental group was 143 mm2 vs. 217 mm2 in control animals. Conclusion: Eker rats fed with ketogenic diet develops solid pituitary adenoma in 14 months of age. Incidence of these pituitary tumors in Eker rats fed with ketogenic diet (8%) was lower when compared with rats from control group (20%).
5

IL-1betta stimulates cytokine secretion by peripheral leukocytes following subarachnoid hemorrhage in rats.

88%
Jedrzejowska-Szypulka H., Woszczycka-Korczynska L., Olakowska E., Larysz-Brysz M., Lewin-Kowalik J.
Acta Neurobiologiae Experimentalis
|
2009
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tom 69
|
nr 3
Much evidence indicates that pathologies observed after subarachnoid hemorrhage (SAH), including vasospasm and neurological defects, are the effects of immuno-infl ammatory processes accompanying the hemorrhage. Following SAH, CSF concentration of cytokines increase, what may change the cerebral perfusion and destroy brain–blood barrier. These cytokines are produced by activated leukocytes as well as hypoxic cells in the brain. The aim of this study was to examine the role of IL-1β in stimulation of peripheral leukocytes to increase secretion of cytokines after SAH. SAH was produced by injection of 150 μL of autologous arterial blood into cisterna magna. In 50% of animals, IL-1β activity was inhibited by intracerebroventricular administration of anti-rat IL-1β antibodies (SAH’ groups). Control group consisted of sham-operated rats. Ninety minutes or 24 h following surgery, blood samples were collected and subpopulations of mononuclear leukocytes were isolated and cultured for 24 h. Then, the concentration of TNF-α, ET-1 and IL-6 in supernatants was measured by means of ELISA. SAH resulted in signifi cant increase in TNF-α and ET-1, especially after 24 h, and no change in IL-6 concentration. Inhibition of IL1-β decreased the secretion of TNF-α and ET-1 and led to increase in IL-6. We found that peripheral leukocytes are an additional source of cytokines following SAH, and their activation depends on IL1-β produced after hemorrhage.
6
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Influence of the corticotropin releasing hormone (CRH) on the brain-blood barrier permeability in cerebral ischemia in rats

88%
Hendryk S., Jedrzejowska-Szypulka H., Josko J., Jarzab B., Dohler K. D.
Journal of Physiology and Pharmacology
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2002
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tom 53
|
nr 1
The increase in the blood-brain barrier (BBB)permeability and a developing cerebral oedema due to the ischemic infarction appear a few hours,and intensify during a few days,after closing the carotid arteries.It fails to be clear,however,what causes the increase in the microvessels damage,and whether the damage is a secondary result of the vasoactive substances released by the neurones and glia cells damaged by the ischemia.CRH,which plays an essential role in integrative the nervous,endocrine, and immunological systems,has a positive effect on the decrease in the permeability of the BBB damaged by various physical and chemical factors.Therefore,the examination of the CRH role in the cerebral ischemia may prove useful for explaining the processes taking place in the foci of the cerebral infarction and their environment. The experiment was carried out on rats which,20 minutes before closing of both internal carotid arteries,was administered 10 µg CRH to cerebrospinal fluid via cisterna magna of the brain.The BBB permeability was measured 30 minutes,3 hours,3 days,and 7 days after closing the arteries.The experiment has shown the CRH protective effect on the BBB and its consequent effect on the decrease in the BBB permeability which appears in the 3 hours after closing the arteries (p<0.05),and is high significant during the chronic phase of the cerebral ischemia (p<0.03).It can be thus concluded that CRH,by affecting directly the endothelium of the cerebral vessels, decreases the endothelial damage in the acute phase of the ischemia.The decrease is noted to be more significant in the chronic phase of the ischemia;such an effect can be attributed to CRH stimulating the hypothalamic-adrenal axis,and to the secondary activation of the mechanisms decreasing the BBB permeability.
7
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Corticotropin releasing hormone [CRH] increases beta-endorphin [beta-end like] concentration in cerebrospinal fluid of rats with vasospasm following subarachnoid hemorrhage

88%
Henryk S., Josko J., Jedrzejowska-Szypulka H., Jarzab B., Dohler K. D.
Journal of Physiology and Pharmacology
|
1999
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tom 50
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nr 3
8

Does restruction of jugular venous outflow induce multiple sclerosis-like signs in rat brains?p.S66-S67

76%
Jedrzejowska-Szypulka H., Kotulska K., Kapustka B., Laczynski M., Larysz-Brysz M., Lewin-Kowalik J.
Acta Neurobiologiae Experimentalis
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2015
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tom 75
|
nr Supl.
BACKGROUND AND AIMS: Hypothesis that multiple sclerosis (MS) may be caused by chronic cerebrospinal venous insufficiency (CCVI) has gained public interest from both patients and physicians. However, there’s still lack of evidence for it. We have investigated presence of neuronal demyelination and degeneration, similar to these found in MS, in rat model of CCVI created by occlusion of jugular veins (JVs). METHODS: Twenty-five young female Wistar C rats were used. Complete ligation of both JVs (BO group), left JV (UO), or partial ligation (stenosis resulting in ~70% reduction of blood flow) of both JVs were performed. Blood flow in JVs was measured with Laser Doppler Flow Assessment. Neurological assessment using Neurologic Deficit Scale (NDS), 5-point EAE staging protocol, and gait analysis with CatWalk was performed. After 12 weeks, MRI for detecting demyelinating plaques as well as signs of bloodbrain barrier (BBB) disruption was performed. Histologic analysis of brain specimens was focused on markers of inflammation and demyelination. RESULTS: No neurologic deficits were found in all experimental animals. Both NDS, EAE and gait analysis did not differ from normal. MRI T2- and T1- weighted imaging as well as FLAIR sequence did not reveal any abnormalities in the brains of experimental rats. Histological analysis did not show any signs of inflammation or demyelination. CONCLUSIONS: Twelve-week CCVI in rats, both complete and partial, did not induce any changes resembling pathologies observed in MS. Therefore, linking CCVI with origin of MS remains controversial.
9

Activated schwann cells delivered into the subarachnoid space via cisterna magna induce repair of injured rat spinal cord white matter

76%
Lewin-Kowalik J., Marcol W., Jedrzejowska-Szypulka H., Slusarczyk W., Smetek J., Sordyl R., Larysz-Brysz M.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
We investigated the influence of activated Schwann cells on regeneration of the spinal cord in rats. Young adult male Wistar C rats were used (n=36). Focal injury of spinal cord white matter at Th10 level was produced using our original non-laminectomy method by means of high-pressured air stream. Schwann cells obtained from 7-days-predegenerated rats’ sciatic nerves (n=3) were cultured, transfected with GFP and injected into cisterna magna (S group, n=23) three times: immediately after spinal cord injury and 3 as well as 7 days later (300 000 cells/injection). Control animals (n=10) were subjected to the spinal cord injury only. Neurons in brain stem and motor cortex were labeled with FluoroGold (FG) delivered caudally from the injury site and transported via spinal ascending tracts a week before the end of experiment. Functional outcome (BBB scale, Sciatic Functional Index) and morphological features of regeneration were analyzed during 12-week follow-up. The lesions were characterized by means of MRI. Maximal distance of expansion of implanted cells in the spinal cord was measured and the number of FG-positive neurons was counted. Rats treated with Schwann cells presented significant improvement of locomotor performance when compared to the control group. MR images showed no cyst in the spinal cord in S group, while in the control group changes resembling typical post-traumatic syringomyelia were found. The sizes of lesions were also significantly smaller in S group. Distance covered by Schwann cells was 12 mm from the epicenter of injury. Number of brain stem and motor cortex FG-positive neurons in S group was significantly higher than in control group. Obtained data revealed that activated Schwann cells are able to induce the repair of injured spinal cord white matter. The route of cells application via cisterna magna appeared useful for their delivery into the injury area.
10
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Influence of 5-aminoisoquinolin-1-one (5-AIQ) on neutrophil chemiluminescence in rats with transient and prolonged focal cerebral ischaemia and after reperfusion

76%
Hendryk S., Czuba Z. P., Jedrzejowska-Szypulka H., Szliszka E., Phillips V. A., Threadgill M. D., Krol W.
Journal of Physiology and Pharmacology
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2008
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tom 59
|
nr 4
811-822
Stimulation of neutrophils by different factors increases their oxidative activity and the free radicals produced can report on the degree of activation. Poly(adenosine 5’-diphosphate ribose)polymerase-1 (PARP-1), a nuclear enzyme activated by strand breaks in DNA, plays an important role in the tissue injury associated with ischaemia-reperfusion injury and inflammation. 5-Aminoisoquinolin-1-one (5-AIQ) is a potent inhibitor of PARP-1 activity in vitro and in vivo in rats. Acute (80 min) and prolonged (24h) focal cerebral ischaemia was induced in rats by obstruction of the median cerebral artery, with or without reperfusion, with or without administration of 5-AIQ. The oxidative activity of neutrophils was measured by chemiluminescence. Administration of 5-AIQ.HCl (3.0 mg kg-1 b.w. - i.v.) caused a significant decrease in the oxidative activity of neutrophils in the group which had experienced chronic ischaemia for 24h but had no significant effect in the group which had received 80 min ischaemia, when compared to the control group. Increase of the oxidative activity of neutrophils was confirmed in rats with prolonged cerebral ischaemia, followed by reperfusion. 5-AIQ probably may decrease this activity through inhibition of PARP-1 in focus of local ischaemia as well as hence lowering the expression of inflammatory mediators by activated neutrophils.
11
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Effect of endothelin-1 receptor antagonist BQ-123 on basilar artery diameter after subarachnoid hemorrhage (SAH) in rats

76%
Josko J., Hendryk S., Jedrzejowska-Szypulka H., Slowinski J., Gwozdz B., Lange D., Harabin-Slowinska M.
Journal of Physiology and Pharmacology
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2000
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tom 51
|
nr 2
12
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Atrial natriuretic peptide secretion following subarachnoid hemorrhage in spontaneously hypertensive rats

76%
Josko J., Hendryk S., Jedrzejowska-Szypulka H., Gwozdz B., Herman Z. S., Latka D., Kopec N.
Journal of Physiology and Pharmacology
|
1996
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tom 47
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nr 4
13
Content available remote

The importance of selected markers of inflammation and blood-brain barrier damage for short-term ischemic stroke prognosis

64%
Lasek-Bal A., Jedrzejowska-Szypulka H., Student S., Warsz-Wianecka A., Zareba K., Puz P., Bal W., Pawletko K., Lewin-Kowalik J.
Journal of Physiology and Pharmacology
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2019
|
tom 70
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nr 2
14
Content available remote

The presence of tau protein in blood as a potential prognostic factor in stroke patients

64%
Lasek-Bal A., Jedrzejowska-Szypulka H., Rozycka J., Bal W., Kowalczyk A., Holecki M., Dulawa J., Lewin-Kowalik J.
Journal of Physiology and Pharmacology
|
2016
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tom 67
|
nr 5
15
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Content available

Cerebral angiogenesis after subarachnoid hemorrhage (SAH) and endothelin receptor blockage with BQ-123 antagonist in rats

64%
Josko J., Hendryk S., Jedrzejowska-Szypulka H., Slowinski J., Gwozdz B., Lange D., Snietura M., Zwirska-Korczala K., Jochem J.
Journal of Physiology and Pharmacology
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2001
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tom 52
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nr 2
16
Content available remote

Concentrations and activities of metalloproteinases 2 and 9 and their inhibitors (TIMPS) in chronic pancreatitis and pancreatic adenocarcinoma

52%
Lekstan A., Lampe P., Lewin-Kowalik J., Olakowski M., Jablonska B., Labuzek K., Jedrzejowska-Szypulka H., Olakowska E., Gorka D., Filip I., Dranka-Bojarowska D.
Journal of Physiology and Pharmacology
|
2012
|
tom 63
|
nr 6
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