共查询到20条相似文献,搜索用时 359 毫秒
1.
Yana O. Mukhamedshina Ekaterina E. Garanina Galina A. Masgutova Luisa R. Galieva Elvira R. Sanatova Yurii A. Chelyshev Albert A. Rizvanov 《PloS one》2016,11(3)
Objective and Methods
This study investigated the potential for protective effects of human umbilical cord blood mononuclear cells (UCB-MCs) genetically modified with the VEGF and GNDF genes on contusion spinal cord injury (SCI) in rats. An adenoviral vector was constructed for targeted delivery of VEGF and GDNF to UCB-MCs. Using a rat contusion SCI model we examined the efficacy of the construct on tissue sparing, glial scar severity, the extent of axonal regeneration, recovery of motor function, and analyzed the expression of the recombinant genes VEGF and GNDF in vitro and in vivo.Results
Transplantation of UCB-MCs transduced with adenoviral vectors expressing VEGF and GDNF at the site of SCI induced tissue sparing, behavioral recovery and axonal regeneration comparing to the other constructs tested. The adenovirus encoding VEGF and GDNF for transduction of UCB-MCs was shown to be an effective and stable vehicle for these cells in vivo following the transplantation into the contused spinal cord.Conclusion
Our results show that a gene delivery using UCB-MCs-expressing VEGF and GNDF genes improved both structural and functional parameters after SCI. Further histological and behavioral studies, especially at later time points, in animals with SCI after transplantation of genetically modified UCB-MCs (overexpressing VEGF and GDNF genes) will provide additional insight into therapeutic potential of such cells. 相似文献2.
W. Kang S. Kim S. Lee E. Jeon Y. Lee Y.R. Yun C.K. Suh H.W. Kim J.H. Jang 《Protein expression and purification》2013,87(2):55-60
Vascular endothelial growth factors165 (VEGF165) is the most potent and widely used pro-angiogenic factor. Here we determined optimal culture condition of recombinant human VEGF165 (rhVEGF165) in Escherichia coli (E. coli). rhVEGF165 expression was the highest in 0.25% of l-arabinose induction concentration, at 20 °C induction temperature, and for 5 h induction time under the control of araBAD promoter using pBADHisA vector. In biological activity test, rhVEGF165 significantly increased the proliferative activity of CPAE cells (p < 0.001) and upregulated the expressions of endothelial cell growth-related genes, such as platelet endothelial cell adhesion molecule (PECAM-1), endothelial-specific receptor tyrosine kinase (TEK), kinase insert domain protein receptor (KDR), and tyrosine kinase with immunoglobulin-like and EGF-like domains 1 (TIE1) in calf pulmonary artery endothelial (CPAE) cells. 相似文献
3.
Sun Kwon Bang Young Sik Kim Byung Soo Chang Cheol Beom Park In Seok Bang 《Biotechnology and Bioprocess Engineering》2013,18(5):835-842
Vascular endothelial growth factors (VEGFs) are a family of proteins that promote angiogenesis and participate in a variety of physiological and pathological processes. In this work, the gene encoding the human VEGF isoform 165 (hVEGF165) was cloned into the expression vector pET32a (+) to construct a fusion expression plasmid that induced the thioredoxin (Trx) gene and transformed into Escherichia coli. The recombinant fusion protein TrxhVEGF165 was expressed optimally as inclusion bodies in the case of being cultivated for 4 h at 30°C and 1 mM IPTG concentration. The Trx-hVEGF165 was refolded and purified effectively from urea-solubilized inclusion bodies by the immobilized metal affinity chromatography. Released from the fusion protein by enterokinase cleavage and purified to homogeneity, the recombinant hVEGF165 (rhVEGF165) was biologically active as assessed by the human umbilicalvein endothelial cells (HUVECs) proliferation and the chicken chorioallantoic membrane (CAM) assay. The expression and in vitro refolding of rhVEGF165 resulted in production of an active molecule in a yield of 4.04 mg/L flask cultivation. 相似文献
4.
血管内皮细胞生长因子(vascular endothelial growth factor, VEGF)是抑制肿瘤生长和转移的重要靶点。为获得抗VEGF单抗细胞株,构建了rhVEGF165工程菌,并利用复合自动诱导获得高效表达。经纯化获得高纯度rhVEGF165蛋白,经检测具有促人脐静脉内皮细胞(human umbilical vein endothelial cells, HUVECs)增殖活性,其EC50为2.4ng/ml。免疫小鼠,获得了3株能稳定分泌抗VEGF单抗的杂交瘤细胞株,为开发VEGF治疗性单抗提供了重要基础。 相似文献
5.
Asrin Rahimi Iraj Amiri Amaneh Mohammadi Roushandeh Zoleikha Golipour Choshali Zohreh Alizadeh Tayebeh Artimani Saeid Afshar Sara Soleimani Asl 《Biotechnology letters》2018,40(3):609-615
Objective
To investigate the effect of H2O2 on the migration and antioxidant defense of mesenchymal stem cells (MSCs) and the neurotrophic effects of H2O2-treated MSCs on spinal cord injury (SCI).Results
Sublethal concentrations of H2O2 decreased cell migration and expression of CXCR4 and CCR2 as well as Nrf2 expression in MSCs. In the second phase, transplantation of treated and untreated MSCs to SCI caused minor changes in locomotor dysfunction. There was a significantly difference between cell-treated and spinal cord injury groups in expression of BDNF (brain-derived neurotrophic factor). Transplantation of H2O2-treated cells caused an increase in BDNF expression compared to non-treated cells.Conclusion
Transplantation of H2O2-treated stem cells may have protective effects against SCI through by increasing neurotrophic factors.6.
Mohsen Azimi-Nezhad 《Reports of Biochemistry & Molecular Biology》2014,2(2):59-69
Vascular endothelial growth factor (VEGF) is a multifunctional cytokine with distinct functions in angiogenesis, lymphangiogenesis, vascular permeability, and hematopoiesis. VEGF is a highly conserved, disulfide-bonded dimeric glycoprotein of 34 to 45 kDa produced by several cell types including fibroblasts, neutrophils, endothelial cells, and peripheral blood mononuclear cells, particularly T lymphocytes and macrophages. Six VEGF isoforms are generated as a result of alternative splicing from a single VEGF gene, consisting of 121, 145, 165, 183, 189, or 206 amino acids. VEGF121, VEGF145, and VEGF165 are secreted whereas VEGF183, VEGF189, and VEGF206 are cell membrane-bound. VEGF145 has a key role during the vascularization of the human ovarian follicle and corpus luteum, in the placentation and embryonic periods, and in bone and wound healing, while VEGF165 is the most abundant and biologically active isoform. VEGF has been linked with a number of vascular pathologies including cardiovascular diseases such ischemic heart disease, heart failure, stroke, and diabetes and its related complications. In this review we aimed to present some important roles of VEGF in a number of clinical issues and indicate its involvement in several phenomena from the initial steps of the embryonic period to cardiovascular diseases. Key Words: Vascular endothelial growth factor (VEGF), Vascular pathogenesis 相似文献
7.
Jonghyuck Park Lingxing Zheng Andrew Marquis Michael Walls Brad Duerstock Amber Pond Sasha Vega‐Alvarez He Wang Zheng Ouyang Riyi Shi 《Journal of neurochemistry》2014,129(2):339-349
Acrolein, an α,β‐unsaturated aldehyde and a reactive product of lipid peroxidation, has been suggested as a key factor in neural post‐traumatic secondary injury in spinal cord injury (SCI), mainly based on in vitro and ex vivo evidence. Here, we demonstrate an increase of acrolein up to 300%; the elevation lasted at least 2 weeks in a rat SCI model. More importantly, hydralazine, a known acrolein scavenger can provide neuroprotection when applied systemically. Besides effectively reducing acrolein, hydralazine treatment also resulted in significant amelioration of tissue damage, motor deficits, and neuropathic pain. This effect was further supported by demonstrating the ability of hydralazine to reach spinal cord tissue at a therapeutic level following intraperitoneal application. This suggests that hydralazine is an effective neuroprotective agent not only in vitro, but in a live animal model of SCI as well. Finally, the role of acrolein in SCI was further validated by the fact that acrolein injection into the spinal cord caused significant SCI‐like tissue damage and motor deficits. Taken together, available evidence strongly suggests a critical causal role of acrolein in the pathogenesis of spinal cord trauma. Since acrolein has been linked to a variety of illness and conditions, we believe that acrolein‐scavenging measures have the potential to be expanded significantly ensuring a broad impact on human health.
8.
9.
Microvascular dysfunction, loss of vascular support, ischaemia and sub-acute vascular instability in surviving blood vessels contribute to secondary injury following SCI (spinal cord injury). Neither the precise temporal profile of the cellular dynamics of spinal microvasculature nor the potential molecular effectors regulating this plasticity are well understood. TGFβ (transforming growth factor β) isoforms have been shown to be rapidly increased in response to SCI and CNS (central nervous system) ischaemia, but no data exist regarding their contribution to microvascular dysfunction following SCI. To examine these issues, in the present study we used a model of focal spinal cord ischaemia/reperfusion SCI to examine the cellular response(s) of affected microvessels from 30 min to 14 days post-ischaemia. Spinal endothelial cells were isolated from affected tissue and subjected to focused microarray analysis of TGFβ-responsive/related mRNAs 6 and 24 h post-SCI. Immunohistochemical analyses of histopathology show neuronal disruption/loss and astroglial regression from spinal microvessels by 3 h post-ischaemia, with complete dissolution of functional endfeet (loss of aquaporin-4) by 12 h post-ischaemia. Coincident with this microvascular plasticity, results from microarray analyses show 9 out of 22 TGFβ-responsive mRNAs significantly up-regulated by 6 h post-ischaemia. Of these, serpine 1/PAI-1 (plasminogen-activator inhibitor 1) demonstrated the greatest increase (>40-fold). Furthermore, uPA (urokinase-type plasminogen activator), another member of the PAS (plasminogen activator system), was also significantly increased (>7.5-fold). These results, along with other select up-regulated mRNAs, were confirmed biochemically or immunohistochemically. Taken together, these results implicate TGFβ as a potential molecular effector of the anatomical and functional plasticity of microvessels following SCI. 相似文献
10.
Embryonic neural stem cell (ENSC) transplantation is used experimentally for the improvement of spinal cord repair following
spinal cord injury (SCI). However, the effects of such intervention on oxidative stress and cell death remain unknown. We
used in vivo Comet assay in the acute and chronic SCI groups compared with the SCI+ENSC transplantation groups of experimental rats in
order to evaluate DNA damage in the spinal cord. Chronic SCI resulted in the generation of oxidative DNA damage in the spinal
cord brain and kidneys, as indicated by high Comet assay parameters, including the percentage of DNA in the tail (T%, or TD),
tail moment (TM), and tail length (TL). The DNA damage levels significantly decreased after ENSC transplantation in the spinal
cords of acute and chronic SCI groups within the lesion site and rostrally and caudally to the injury, and in the brains and
kidneys of the chronic SCI group. Thus, ENSC transplantation is found to be an effective tool for limitation of DNA damage
following spinal cord injury. 相似文献
11.
Ryo Kadota Masao Koda Junko Kawabe Masayuki Hashimoto Yutaka Nishio Chikato Mannoji Tomohiro Miyashita Takeo Furuya Akihiko Okawa Kazuhisa Takahashi Masashi Yamazaki 《PloS one》2012,7(11)
Background
Granulocyte colony-stimulating factor (G-CSF) is a protein that stimulates differentiation, proliferation, and survival of cells in the granulocytic lineage. Recently, a neuroprotective effect of G-CSF was reported in a model of cerebral infarction and we previously reported the same effect in studies of murine spinal cord injury (SCI). The aim of the present study was to elucidate the potential therapeutic effect of G-CSF for SCI in rats.Methods
Adult female Sprague-Dawley rats were used in the present study. Contusive SCI was introduced using the Infinite Horizon Impactor (magnitude: 200 kilodyne). Recombinant human G-CSF (15.0 µg/kg) was administered by tail vein injection at 1 h after surgery and daily the next four days. The vehicle control rats received equal volumes of normal saline at the same time points.Results
Using a contusive SCI model to examine the neuroprotective potential of G-CSF, we found that G-CSF suppressed the expression of pro-inflammatory cytokine (IL-1 beta and TNF- alpha) in mRNA and protein levels. Histological assessment with luxol fast blue staining revealed that the area of white matter spared in the injured spinal cord was significantly larger in G-CSF-treated rats. Immunohistochemical analysis showed that G-CSF promoted up-regulation of anti-apoptotic protein Bcl-Xl on oligpodendrocytes and suppressed apoptosis of oligodendrocytes after SCI. Moreover, administration of G-CSF promoted better functional recovery of hind limbs.Conclusions
G-CSF protects oligodendrocyte from SCI-induced cell death via the suppression of inflammatory cytokines and up-regulation of anti-apoptotic protein. As a result, G-CSF attenuates white matter loss and promotes hindlimb functional recovery. 相似文献12.
13.
Young-sup Yoon Ingrid A. Johnson Jong-Seon Park Larry Diaz Douglas W. Losordo 《Molecular and cellular biochemistry》2005,264(1-2):63-74
Emerging evidence has shown that administration of angiogenic growth factors, either as recombinant protein or by gene transfer, can augment tissue perfusion through neovascularization in animal models of myocardial and hindlimb ischemia. Many cytokines have angiogenic activity; one of those that have been best studied in animal models and clinical trials is vascular endothelial growth factor (VEGF). VEGF has been known to be a key regulator of physiologic and pathologic angiogenesis associated with tumor. Recently the effect of VEGF is not restricted to the direct angiogenic effect in vivo but includes mobilization of bone-marrow-derived endothelial progenitor cells and augmentation of postnatal vasculogenesis in situ. Clinical trials of therapeutic angiogenesis with VEGF in patients with end-stage coronary artery disease have shown increases in exercise time and reductions in anginal symptoms and have provided objective evidence of improved perfusion and left ventricular function. Larger scale placebo-controlled trials with recombinant protein (rhVEGF165) have been limited to intracoronary and intravenous administration and have shown favorable trends in exercise time and angina frequency. Small-scale, placebo-controlled, randomized clinical trials of gene transfer (phVEGF-2) via thoracotomy or percutaneous intramyocardial delivery demonstrated significant improvement of both subjective symptoms and objective measures of myocardial ischemia. Both therapeutic modalities appear to be safe and well tolerated. Further studies are required to determine the optimal dose, formulation, route of administration, and combinations of growth factors and the utility of adjunctive endothelial progenitor cell or other stem cell supplementation, to provide safe and effective therapeutic myocardial neovascularization. (Mol Cell Biochem 264: 63–74, 2004) 相似文献
14.
Protective role of vascular endothelial growth factor in endotoxin-induced acute lung injury in mice
Hidefumi Koh Sadatomo Tasaka Naoki Hasegawa Wakako Yamada Mie Shimizu Morio Nakamura Makoto Yonemaru Eiji Ikeda Yoshiyuki Adachi Seitaro Fujishima Kazuhiro Yamaguchi Akitoshi Ishizaka 《Respiratory research》2007,8(1):60-13
Background
Vascular endothelial growth factor (VEGF), a substance that stimulates new blood vessel formation, is an important survival factor for endothelial cells. Although overexpressed VEGF in the lung induces pulmonary edema with increased lung vascular permeability, the role of VEGF in the development of acute lung injury remains to be determined.Methods
To evaluate the role of VEGF in the pathogenesis of acute lung injury, we first evaluated the effects of exogenous VEGF and VEGF blockade using monoclonal antibody on LPS-induced lung injury in mice. Using the lung specimens, we performed TUNEL staining to detect apoptotic cells and immunostaining to evaluate the expression of apoptosis-associated molecules, including caspase-3, Bax, apoptosis inducing factor (AIF), and cytochrome C. As a parameter of endothelial permeability, we measured the albumin transferred across human pulmonary artery endothelial cell (HPAEC) monolayers cultured on porous filters with various concentrations of VEGF. The effect of VEGF on apoptosis HPAECs was also examined by TUNEL staining and active caspase-3 immunoassay.Results
Exogenous VEGF significantly decreased LPS-induced extravascular albumin leakage and edema formation. Treatment with anti-VEGF antibody significantly enhanced lung edema formation and neutrophil emigration after intratracheal LPS administration, whereas extravascular albumin leakage was not significantly changed by VEGF blockade. In lung pathology, pretreatment with VEGF significantly decreased the numbers of TUNEL positive cells and those with positive immunostaining of the pro-apoptotic molecules examined. VEGF attenuated the increases in the permeability of the HPAEC monolayer and the apoptosis of HPAECs induced by TNF-α and LPS. In addition, VEGF significantly reduced the levels of TNF-α- and LPS-induced active caspase-3 in HPAEC lysates.Conclusion
These results suggest that VEGF suppresses the apoptosis induced by inflammatory stimuli and functions as a protective factor against acute lung injury. 相似文献15.
Upregulation of vascular endothelial growth factor receptors Flt-1 and Flk-1 following acute spinal cord contusion in rats. 总被引:2,自引:0,他引:2
Jeong-Sun Choi Ha-Young Kim Jung-Ho Cha Jae-Youn Choi Sang In Park Chang Hyun Jeong Sin-Soo Jeun Mun-Yong Lee 《The journal of histochemistry and cytochemistry》2007,55(8):821-830
To investigate the possible role of vascular endothelial growth factor (VEGF) in the injured spinal cord, we analyzed the distribution and time course of the two tyrosine kinase receptors for VEGF, Flt-1 and Flk-1, in the rat spinal cord following contusion injury using a weight-drop impactor. The semi-quantitative RT-PCR analysis of Flt-1 and Flk-1 in the spinal cord showed slight upregulation of these receptors following spinal cord injury. Although mRNAs for Flt-1 and Flk-1 were constitutively expressed in neurons, vascular endothelial cells, and some astrocytes in laminectomy control rats, their upregulation was induced in association with microglia/macrophages and reactive astrocytes in the vicinity of the lesion within 1 day in rats with a contusion injury and persisted for at least 14 days. The spatiotemporal expression of Flt-1 in the contused spinal cord mirrored that of Flk-1 expression. In the early phase of spinal cord injury, upregulation of Flt-1 and Flk-1 mRNA occurred in microglia/macrophages that infiltrated the lesion. In addition, the expression of both receptors increased progressively in reactive astrocytes within the vicinity of the lesion, predominately in the white matter, and almost all reactive astrocytes coexpressed Flt-1 or Flk-1 and nestin. These results suggest that VEGF may be involved in the inflammatory response and the astroglial reaction to contusion injuries of the spinal cord via specific VEGF receptors. 相似文献
16.
Armin Buss Katrin Pech Byron A Kakulas Didier Martin Jean Schoenen Johannes Noth Gary A Brook 《BMC neurology》2009,9(1):32-15
Background
A major class of axon growth-repulsive molecules associated with CNS scar tissue is the family of chondroitin sulphate proteoglycans (CSPGs). Experimental spinal cord injury (SCI) has demonstrated rapid re-expression of CSPGs at and around the lesion site. The pharmacological digestion of CSPGs in such lesion models results in substantially enhanced axonal regeneration and a significant functional recovery. The potential therapeutic relevance of interfering with CSPG expression or function following experimental injuries seems clear, however, the spatio-temporal pattern of expression of individual members of the CSPG family following human spinal cord injury is only poorly defined. In the present correlative investigation, the expression pattern of CSPG family members NG2, neurocan, versican and phosphacan was studied in the human spinal cord.Methods
An immunohistochemical investigation in post mortem samples of control and lesioned human spinal cords was performed. All patients with traumatic SCI had been clinically diagnosed as having "complete" injuries and presented lesions of the maceration type.Results
In sections from control spinal cord, NG2 immunoreactivity was restricted to stellate-shaped cells corresponding to oligodendrocyte precursor cells. The distribution patterns of phosphacan, neurocan and versican in control human spinal cord parenchyma were similar, with a fine reticular pattern being observed in white matter (but also located in gray matter for phosphacan). Neurocan staining was also associated with blood vessel walls. Furthermore, phosphacan, neurocan and versican were present in the myelin sheaths of ventral and dorsal nerve roots axons. After human SCI, NG2 and phosphacan were both detected in the evolving astroglial scar. Neurocan and versican were detected exclusively in the lesion epicentre, being associated with infiltrating Schwann cells in the myelin sheaths of invading peripheral nerve fibres from lesioned dorsal roots.Conclusion
NG2 and phosphacan were both present in the evolving astroglial scar and, therefore, might play an important role in the blockade of successful CNS regeneration. Neurocan and versican, however, were located at the lesion epicentre, associated with Schwann cell myelin on regenerating peripheral nerve fibres, a distribution that was unlikely to contribute to failed CNS axon regeneration. The present data points to the importance of such correlative investigations for demonstrating the clinical relevance of experimental data. 相似文献17.
Summary. The neuroprotective efficacy of growth hormone on a focal spinal cord trauma induced alteration in the blood-spinal cord
barrier (BSCB) and edema formation was examined in a rat model. Under Equithesin anaesthesia, one segment laminectomy was
done over the T10–11 segments. Spinal cord injury was produced by making an incision into the right dorsal horn of the T10–11
segments (2 mm deep and 4 mm long). The animals were allowed to survive 5 h after injury. Highly purified rat growth hormone
[rGH, 25 μl of a 1 μg/ml solution) was applied over 10 sec topically on the exposed surface of the spinal cord 30 min before injury. The identical
doses of the rGH were repeated 0 min, 30 min, 60 min, 120 min, 180 min and 240 min following injury. Saline (0.9% NaCl) treated
traumatised rats at identical intervals served as controls. Traumatised rats treated with saline exhibited marked edema formation
and extravasation of Evans blue and [125]Iodine tracers in the spinal cord. At the ultrastructural level, perivascular edema and exudation of lanthanum across the
endothelial cells was quite frequent in the spinal cord. Pretreatment with rGH significantly attenuated the edema formation
and the extravasation of tracers in the spinal cord. In these rats, perivascular edema and infiltration of lanthanum across
the endothelial cells was not much evident. These observations show that the rGH has the capacity to reduce the early manifestations
of microvascular permeability disturbances and edema formation following trauma and further suggest a possible therapeutic
potential of the hormone for the treatment of spinal cord injuries.
Received July 3, 2001 Accepted August 6, 2001 Published online July 31, 2002 相似文献
18.
Arnaud Dubory Elisabeth Laemmel Anna Badner Jacques Duranteau Eric Vicaut Charles Court Marc Soubeyrand 《Journal of visualized experiments : JoVE》2015,(99)
Reduced spinal cord blood flow (SCBF) (i.e., ischemia) plays a key role in traumatic spinal cord injury (SCI) pathophysiology and is accordingly an important target for neuroprotective therapies. Although several techniques have been described to assess SCBF, they all have significant limitations. To overcome the latter, we propose the use of real-time contrast enhanced ultrasound imaging (CEU). Here we describe the application of this technique in a rat contusion model of SCI. A jugular catheter is first implanted for the repeated injection of contrast agent, a sodium chloride solution of sulphur hexafluoride encapsulated microbubbles. The spine is then stabilized with a custom-made 3D-frame and the spinal cord dura mater is exposed by a laminectomy at ThIX-ThXII. The ultrasound probe is then positioned at the posterior aspect of the dura mater (coated with ultrasound gel). To assess baseline SCBF, a single intravenous injection (400 µl) of contrast agent is applied to record its passage through the intact spinal cord microvasculature. A weight-drop device is subsequently used to generate a reproducible experimental contusion model of SCI. Contrast agent is re-injected 15 min following the injury to assess post-SCI SCBF changes. CEU allows for real time and in-vivo assessment of SCBF changes following SCI. In the uninjured animal, ultrasound imaging showed uneven blood flow along the intact spinal cord. Furthermore, 15 min post-SCI, there was critical ischemia at the level of the epicenter while SCBF remained preserved in the more remote intact areas. In the regions adjacent to the epicenter (both rostral and caudal), SCBF was significantly reduced. This corresponds to the previously described “ischemic penumbra zone”. This tool is of major interest for assessing the effects of therapies aimed at limiting ischemia and the resulting tissue necrosis subsequent to SCI. 相似文献
19.
Summary. Dynorphin is a neuropeptide that is present in high quantities in the dorsal horn of the spinal cord. The peptide is actively
involved in pain processing pathways. However, its involvement in spinal cord injury is not well known. Alteration in dynorphin
immunoreactivity occurs following a focal trauma to the rat spinal cord. Infusion of dynorphin into the intrathecal space
of the cord results in ischemia, cell damage and abnormal motor function. Antibodies to dynorphin when injected into the intrathecal
space of the spinal cord following trauma improve motor recovery, reduce edema and cell changes. However, influence of dynorphin
on trauma induced alteration in spinal cord bioelectrical activity is still not known. Spinal cord evoked potentials (SCEP)
are good indicator of spinal cord pathology following trauma. Therefore, in present investigation, influence of dynorphin
antibodies on trauma induced changes in SCEP were examined in our rat model. In addition, spinal cord edema formation, microvascular
permeability disturbances and cell injury were also investigated. Our results show that topical application of dynorphin antiserum
(1 : 200) two min before injury markedly attenuated the SCEP changes immediately after injury. In the antiserum treated animals,
a significant reduction in the microvascular permeability, edema formation and cell injury was observed in the traumatised
spinal cord. These observations suggest that (i) dynorphin is involved in the altered bioelectrical activity of the spinal
cord following trauma, (ii) the peptide actively participates in the pathophysiological processes of cell injury in the spinal
cord trauma, and (iii) the dynorphin antiserum has potential therapeutic value for the treatment of spinal cord injuries.
Received July 3, 2001 Accepted August 6, 2001 Published online July 31, 2002 相似文献
20.
Patrick Freund Torben Schneider Zoltan Nagy Chloe Hutton Nikolaus Weiskopf Karl Friston Claudia A. Wheeler-Kingshott Alan J. Thompson 《PloS one》2012,7(12)