Wyniki wyszukiwania

1

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Pathophysiology of ischemic reperfusion injury and the molecular targets involved in amelioration of brain injury by herbal medicine

100%

Badamasi I. M.

Journal of Pre-Clinical and Clinical Research

|

2021

|

tom 15

|

nr 2

2

Novel mechanisms of neurogenesis and neural repair

100%

Gotz M.

Acta Neurobiologiae Experimentalis

|

2019

|

tom 79

|

nr Suppl.1

We study the mechanisms of neurogenesis in order to implement them for neuronal repair. I will present unpublished work about the molecular function of Trnp1, a novel nuclear protein, with key roles in promoting neural stem cell self‑renewal and neurogenesis. Trnp1 shows unprecedented functions in regulating several nuclear processes by its N-terminal intrinsically disordered region, which is highly conserved in mammals. I will then show that Trnp1 is also critical for direct neuronal reprogramming and provide an update on the recent breakthrough in direct glia-to-neuron conversion after brain injury. I will then move on to discuss the integration of replaced neurons into the circuitry of the murine cerebral cortex – that normally does not integrate new neurons at adult stages – and present unpublished data about the mechanisms regulating this integration. Taken together, our knowledge about basic mechanisms of neurogenesis allows us to make great strides towards neuronal repair.

3

Glial scar instability after brain injury

100%

Frontczak-Baniewicz M., Walski M.

Journal of Physiology and Pharmacology. Supplement

|

2006

|

tom 57

|

nr 4

97-102

Glial scar is formed following surgical damage to the cerebral cortex. In the present study we examined the ultrastructural status of the cerebral cortex 14 to 180 days following surgical damage to cerebral parenchyma. The results showed a contribution of astrocytes, but also mesodermal cells, to the process of scar formation. Furthermore, our study showed that the process initiated by trauma did not terminate with the formation of a glial scar. Late phases of repair following tissue damage were associated with lytic processes and a disassembly of the cerebral parenchyma. These findings indicate a changing and unstable nature of the glial scar and its components.

4

Changes in the distribution of immunoglobulin G cellular uptake in the injured cerebral hemisphere in mice

100%

Janeczko K., Pawlinski R., Setkowicz Z.

Folia Histochemica et Cytobiologica

|

1993

|

tom 31

|

nr 4

5

New vessel formation after surgical brain injury in the rat's cerebral cortex. II. Formation of the blood vessels distal to the surgical injury

100%

Walski M., Frontczak-Baniewicz M.

Acta Neurobiologiae Experimentalis

|

2003

|

tom 63

|

nr 2

6

Influence of acute cerebellar lesions on somatosensory evoked potentials (SEPs) in cats

100%

Kolodziejak A., Dziduszko J., Niechaj A., Tarnecki R.

Journal of Physiology and Pharmacology

|

2000

|

tom 51

|

nr 1

7

Spectral analysis of cerebellar activity after acute brain injury in anesthetized rats

100%

Culic M., Blanusa L. M., Grbic G., Spasic S., Jankovic B., Kalauzi A.

Acta Neurobiologiae Experimentalis

|

2005

|

tom 65

|

nr 1

8

Traumatic brain injury results in a concomitant increase in neocortical expression of vasopressin and its V1A receptor

84%

Pascale C. L., Szmydynger-Chodobska J., Sarri J. E., Chodobski A.

Journal of Physiology and Pharmacology. Supplement

|

2006

|

tom 57

|

nr 11

161-167

Arginine vasopressin (AVP) has been shown to promote the disruption of the blood-brain barrier (BBB) and the formation of edema in various animal models of brain injury. However, the source(s) of this AVP have not been identified. Since the cerebral cortex was considerably affected in some of these brain injury models, we sought to determine if AVP was produced in the cerebral cortex, and, if so, whether or not this cortical AVP expression was up regulated after injury. In the present study, a controlled cortical impact model of traumatic brain injury (TBI) in rats was used, and the temporal changes in expression of AVP and its V1a receptor were analyzed by real-time reverse-transcriptase polymerase chain reaction. The expression of AVP and its V1a receptor in the ipsilateral cortex adjacent to the lesion area was significantly up regulated between 4 h and 1day post-TBI. The maximum increase in mRNA for AVP (4.3-fold) and its receptor (2.6-fold) in the ipsilateral vs. contralateral cortex was observed at 6 h post-TBI. Compared to sham-injured rats, no statistically significant changes in expression of AVP or its receptor were found in the contralateral cortex. These results suggest that the cerebral cortex is an important source of AVP in the injured brain, and the parallel increase in the expression of AVP and its cognate receptor may act to augment the actions of AVP related to promoting the disruption of the BBB and the formation of post-traumatic edema.

9

Hypobaric hypoxia and hyperbaric treatment prevents neuronal damage and affect antioxidative activity in neonatal hypoxia-ischemia rat model

84%

Gamdzyk M., Ziembowicz A., Salinska E.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Hypoxic–ischemic encephalopathy (HIE) remains a serious condition that causes significant mortality and long-term morbidity. The aim of the study was to evaluate the effect of hyperbaric oxygen (HBO), hyperbaric air (HBA) and hypobaric hypoxia (HH) on neonatal hypoxic–ischemic (HI) brain injury within a therapeutic window of 1–6 h. We used an experimental model of perinatal hypoxia–ischemia on 7-days old rats, where left (ipsilateral) common carotid artery ligation is followed by 75 min hypoxia. HBO, HBA (2.5 ATA) and HH (0.5 atm air) were applied at 1, 3 or 6 h after HI for 60 min. Treatment was repeated for 3 following days. Brain injury was assessed by comparing ipsilateral hemisphere and contralateral hemisphere weight. Based on the evaluation of weight ratio, HH, HBO and HBA treatment, regardless of time of treatment initiation, resulted in significant reduction of brain weight loss. We observed that HBO reduced brain damage by 58.1%, 57.6% and 54.9%, respectively to the time of treatment initiation (1, 3, 6 h after HI), HBA decreased the damage by 29.9%, 38.1% and 22.0% (respectively). HH also significantly lessened brain weight loss, from 38% after untreated hypoxia–ischemia to 12.9%, 23.1% and 23.8% after HH application respectively 1, 3 and 6 h after hypoxia–ischemia. Superoxide dismutase (SOD) activity and glutathione (GSH) concentration were also measured. HI caused decrease in GSH concentration and 6-fold increase in SOD activity in ipsilateral, but not contralateral hemisphere. HBO treatment applied 1 and 3 h after HI significantly increased GSH concentration and decreased SOD activity, the effect of HBA was less pronounced. HH treatment resulted in additional increase in SOD activity in both hemispheres. However, GSH concentration after HH returned to control values. HBO and HBA altered the expression of cytoplasmic SOD1, and these changes corresponded to changes in SOD activity, suggesting significant role of this protein in neuroprotecting properties of HBO. Our results suggest that HBO, HBA and HH may serve in attenuation of the effects of HI. Early treatment gives better results in brain protection. Our results suggest that HBO and HBA probably reduce synthesis of free oxygen radicals, which manifests in decreased SOD activity. HH however, seems to act on different mechanism, because it enhances SOD activity. It may be beneficial, as it helps to neutralize superoxide anion production, provided that this SOD activity increase is accompanied by activation of glutathione peroxidase (GPx) and catalase (CAT). This assumption needs further investigation.

10

Stable gastric pentadecapeptide BPC 157 heals cysteamine-colitis and colon-colon-anastomosis and counteracts cuprizone brain injuries and motor disability

84%

Klicek R., Kolenc D., Suran J., Drmic D., Brcic L., Aralica G., Sever M., Holjevac J., Radic B., Turudic T., Kokot A., Patrij L., Rucman R., Seiwerth S., Sikiric P.

Journal of Physiology and Pharmacology

|

2013

|

tom 64

|

nr 5

11

The effects of ketogenic and calorie restricted diets on epileptic seizure in rats with mechanical brain injury

84%

Osoba J., Setkowicz-Janeczko Z., Gzielo-Jurek K., Kielbinski M.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Traumatic brain injury (TBI) is a major cause of mortality and morbidity in children and young adults. It initiates multiple cascades of events that lead to acute metabolic dysfunction and cellular energy crisis. TBI remains one of the most common and important causes of acquired epilepsy nowadays. The ketogenic diet (KD) is a specialized high-fat low-protein and low-carbohydrate diet which mimics the anticonvulsive effects of fasting, which were known to suppress seizures. KD is used primarily in children with seizures refractory to standard anticonvulsive drugs (AEDs). Many studies on the anticonvulsant effects of a KD have been performed. Unfortunately, the mechanism of action of the ketogenic diet remains unclear. Although the ketogenic diet is the best dietary therapy for epilepsy, there are other possible approaches including overall restriction of caloric intake. Dietary restriction seems a promising alternative to classic ketogenic diet, possibly because it is associated with higher levels of ketone bodies, which are themselves neuroprotective. Caloric restriction (CR) is defined as a decrease in energy intake without lowering nutritional value. CR improves behavioral outcomes after ischemic brain injury in rats and could possibly act as a neuroprotective factor in global ischemia. It has been also shown that chronic administration of CR may provide protection in the event of TBI. The aim of this research was to study the changes in susceptibility to pilocarpine-induced epileptic seizures in rats with mechanical brain injury. In 30-day-old male Wistar rats (P30), mechanical brain injury was performed. Immediately after, the calorically unrestricted ketogenic diet (KD) and calorically restricted standard laboratory rat chow diet (CR) were introduced. In order to check how the ketogenic diet and caloric restriction alone influence the epileptic seizure susceptibility, two groups of 30-day-old rats were fed KD and CR untill postnatal day 60. At that time, seizures were induced by pilocarpine injection. During the following 6-h period, the animals were continuously observed and motor seizures intensity were rated on a 6-point scale. We have found that KD, both alone or administered to animals with history of experimental brain injury, significantly increases the maximum intensity of pilocarpine-induced seizures, compared to CR fed healthy and injured controls, respectively. Surprisingly, KD and CR seem to have opposite effects in healthy animals as well as animals with a history of experimental brain injury. We have found that KD increases the maximum intensity of pilocarpine-induced seizures, compared to both calorically restricted and unrestricted normal diets. CR, on the other hand, decreases the seizure-genic effect of pilocarpine. This results in a continuum in which calorically restricted animals exhibit the weakest, and KD-fed animals the strongest seizures. To our knowledge, the effects of calorically-restricted and ketogenic diets on pilocarpine-induced seizures have not been previously studied. In other well established models of epilepsy, KD either attenuates or has little effect on seizure intensity.

12

Circadian rhythms of melatonin and cortisol in manifest Huntington's disease and in acute cortical ischemic stroke

84%

Adamczak-Ratajczak A., Kupsz J., Owecki M., Zielonka D., Sowinska A., Checinska-Maciejewska Z., Krauss H., Michalak S., Gibas-Dorna M.

Journal of Physiology and Pharmacology

|

2017

|

tom 68

|

nr 4

13

The proliferative activity of astrocytes after immunoglobulin G uptake in the injured mouse cerebral hemisphere

84%

Janeczko K.

Folia Histochemica et Cytobiologica

|

1994

|

tom 32

|

nr 4

14

Spatio-temporal pattern of proliferation of immunoglobulin G - containing astrocytes in the injured mouse cerebral hemisphere

84%

Janeczko K.

Folia Histochemica et Cytobiologica

|

1995

|

tom 33

|

nr 3

15

New vessel formation after surgical brain injury in the rat's cerebral cortex. I. Formation of the blood vessels proximally to the surgical injury

84%

Frontczak-Baniewicz M., Walski M.

Acta Neurobiologiae Experimentalis

|

2003

|

tom 63

|

nr 2

16

Prophylaxis with alpha-lipoic acid against lipopolysaccharide-induced brain injury in rats

67%

Goraca A., Aslanowicz-Antkowiak K.

Archivum Immunologiae et Therapiae Experimentalis

|

2009

|

tom 57

|

nr 2

141-146

17

Diversity of immunophenotypes of endothelial cells participating in new vessel formation following surgical rat brain injury

67%

Frontczak-Baniewicz M., Walski M., Sulejczak D.

Journal of Physiology and Pharmacology. Supplement

|

2007

|

tom 58

|

nr 5

18

Hydrogen gas reduces brain injury in a global cerebral ischemia model

67%

Ostrowski R. P., Mansell C., Zhang J. H.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Transient global cerebral ischemia-reperfusion injury can occur during acute severe hypotensive states and in cardiac arrest that is followed by resuscitation. This transient reduction in perfusion causes an insult to selective hippocampal neuronal populations via an apoptotic mechanism. Hydrogen gas has a neuroprotective effect and could be used as a pharmacologic agent of beneficial effect. As such we set out in this study to describe the effect of the inhalation of 2.9% hydrogen enriched air following an ischemia-reperfusion injury. A 2-vessel occlusion model was used to induce global cerebral ischemia for 6 minutes while maintaining a hypotensive state with a mean arterial pressure of 30 mm Hg through reversible exsanguinations in male Sprague-Dawley rats (280–330 g). The study included three groups: global ischemia without treatment (GI, n=6), global ischemia with hydrogen (GI + H2, n=6 ) and sham surgery (Sham, n=6). Rats in the treatment group received 2.9% inhalational hydrogen for 1 hour starting 15 minutes following reperfusion. Neurobehavioral testing was performed on day one and T-maze testing prior to being euthanized on days 3 or 7. Treated rats demonstrated an improved outcomes in spontaneous alternations, seizure incidence and survivability. Quantitative Nissl histology and TUNEL of the CA-1 region of the hippocampus showed increased cell survival in the treatment group. We conclude that treatment with inhalational hydrogen following ischemia-reperfusion injury could be low cost method of decreasing the effects of neuronal cell death.

19

Oxygen-glucose deprivation (OGD) promotes microglia activation and gliogenesis but not neurogenesis in organotypic hippocampal slice culture (OHC)

67%

Ziemka-Nalecz M., Wojcik-Stanaszek L., Zajac H., Zalewska T.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Organotypic hippocampal cultures are used as an alternative model for studying molecular mechanism(s) of neurogenesis after combined oxygen-glucose deprivation (OGD) mimicking ischemic conditions. The aim of the present work was to investigate the effect of OGD on stem/progenitor cells proliferation and/or differentiation in the hippocampus. Our attention was primarily focused on the relationship between neurogenesis-associated processes and activity of matrix metalloproteinases (MMPs). Cell proliferation was detected by using BrdU incorporation. Newly generated BrdU (+) cells were identified by labeling with specific cell markers. In order to check the activity and localization of MMPs we conducted in situ zymography in conjunction with immunohistochemistry. In our experimental conditions OGD-insult followed by 24 h of recovery caused the damage of neuronal cells in CA1. At 1 week cell death appears all over the hippocampus. We found that expected stimulation of endogenous neurogenesis fails as a source of compensation for the lost neurons in OGD-treated cultures. The modulation of culture microenvironment after ischemia favors the dominant proliferation of glial cells expressed by the enhancement of newly-generated oligodendrocyte progenitors. In addition, during our study we also detected some BrdU labeled nuclei encapsulated by GFAP positive processes. However, the majority of BrdU positive cells expressed microglial specific stain, particularly pronounced in CAlarea. The OGD-promoted responses involved activation of metalloproteinases, which matches the progression of gliogenesis. On the other hand, the high activity of MMPs associated with microglial cells implicate their involvement in the mechanism participating in OGD-induced cell damage.

20

Difluoromethylornithine counteracts lesion-induced astrogliosis in rat hippocampus : enhancement of inhibitory effect by combined treatment with GM1 ganglioside

67%

Jeglinski W., Skup M., Zaremba M., Oderfeld-Nowak B.

Acta Neurobiologiae Experimentalis

|

1996

|

tom 56

|

nr 2

Ograniczanie wyników

Pathophysiology of ischemic reperfusion injury and the molecular targets involved in amelioration of brain injury by herbal medicine

Novel mechanisms of neurogenesis and neural repair

Glial scar instability after brain injury

Changes in the distribution of immunoglobulin G cellular uptake in the injured cerebral hemisphere in mice

New vessel formation after surgical brain injury in the rat's cerebral cortex. II. Formation of the blood vessels distal to the surgical injury

Influence of acute cerebellar lesions on somatosensory evoked potentials (SEPs) in cats

Spectral analysis of cerebellar activity after acute brain injury in anesthetized rats

Traumatic brain injury results in a concomitant increase in neocortical expression of vasopressin and its V1A receptor

Hypobaric hypoxia and hyperbaric treatment prevents neuronal damage and affect antioxidative activity in neonatal hypoxia-ischemia rat model

Stable gastric pentadecapeptide BPC 157 heals cysteamine-colitis and colon-colon-anastomosis and counteracts cuprizone brain injuries and motor disability

The effects of ketogenic and calorie restricted diets on epileptic seizure in rats with mechanical brain injury

Circadian rhythms of melatonin and cortisol in manifest Huntington's disease and in acute cortical ischemic stroke

The proliferative activity of astrocytes after immunoglobulin G uptake in the injured mouse cerebral hemisphere

Spatio-temporal pattern of proliferation of immunoglobulin G - containing astrocytes in the injured mouse cerebral hemisphere

New vessel formation after surgical brain injury in the rat's cerebral cortex. I. Formation of the blood vessels proximally to the surgical injury

Prophylaxis with alpha-lipoic acid against lipopolysaccharide-induced brain injury in rats

Diversity of immunophenotypes of endothelial cells participating in new vessel formation following surgical rat brain injury

Hydrogen gas reduces brain injury in a global cerebral ischemia model

Oxygen-glucose deprivation (OGD) promotes microglia activation and gliogenesis but not neurogenesis in organotypic hippocampal slice culture (OHC)

Difluoromethylornithine counteracts lesion-induced astrogliosis in rat hippocampus : enhancement of inhibitory effect by combined treatment with GM1 ganglioside