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PubMed1999

Does microcirculation play a role in the pathogenesis of inflammatory bowel diseases? Answers from intravital microscopic studies in animal models.

The potential role of intestinal microcirculation for the development of inflammatory bowel diseases (IBD) has not been systematically investigated, mainly because of methodological problems. Using a well-established rodent model of IBD and intravital microscopy, the present study investigated whether (and when) gut microcirculation is disturbed in IBD, and whether microcirculatory disorders contribute to histological and functional alterations in the development of IBD. Colitis was induced by rectal injection of trinitrobenzene sulfonic acid. After 1, 3, and 15 days rats were laparotomized for intravital microscopic determination of mucosal colonic blood flow. In a second series it was examined whether enhancing colonic capillary blood flow by hemodilution therapy stabilizes colonic wall resistance and other electrophysiological parameters of gut permeability. Additional measurements involved hemodynamic monitoring and histological examinations. Colonic capillary blood flow was significantly decreased 3 days after colitis induction (1.8 +/- 0.05 vs. 2.6 +/- 0.04 nl/min in healthy control animals) when histology revealed signs of acute inflammation, and normal values after 15 days (2.4 +/- 0.06 nl/min) when chronic histological changes were evident. Hemodilution therapy enhanced colonic capillary blood flow in the initial stage (2.1 +/- 0.02 vs. 1.6 +/- 0.02 nl/min in saline-treated animals with trinitrobenzene sulfonic acid colitis) and improved gut resistance and electronic chloride secretion (73 +/- 15 vs. 33 +/- 8 microA cm2). Histological alterations were not significantly attenuated. Impaired colonic capillary blood flow in the initial stage of experimental colitis and improved mucosal microcirculation with stabilized gut permeability suggests that the early microcirculatory disturbances precede chronic histological changes and influence functional alterations in the course of the disease. Research should be continued in this field because important mechanisms in the pathogenesis of IBD and potentially therapeutic (vasoactive) substances may otherwise be overlooked.

Animals↗
PubMed1998

Role of constitutive nitric oxide synthase and peroxynitrite production in a rat model of splanchnic artery occlusion shock.

Peroxynitrite, a potent cytotoxic oxidant formed by the reaction of nitric oxide with superoxide anion, is an important mediator of reperfusion injury. In a rodent model of mesenteric ischemia and reperfusion injury we evaluated the contribution of the constitutive and/or inducible nitric oxide synthase (cNOS or iNOS) in the formation of peroxynitrite. Splanchnic artery occlusion (SAO) shock was induced in rats by clamping both the superior mesenteric artery and the celiac trunk for 45 min, followed by release of the clamps (reperfusion). A significant peroxynitrite production was found in the plasma of the splanchnic occlusion shocked rats at 60 minutes after reperfusion. Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine, a specific "footprint" of peroxynitrite, in the necrotic ileum and the aorta of shocked rats. No change in plasma levels of nitrate/nitrite, tissue iNOS expression (by western blotting detection) or iNOS activity was found in the intestine at 60 minutes after reperfusion. On the contrary, activity of the cNOS was reduced (approximately 50%) in the reperfused ischemic intestinal tissue. Treatment with NG-nitro-L-arginine methyl ester, a non selective inhibitor of nitric oxide synthase (given at 3 mg/kg i.v., 5 min prior to reperfusion), significantly reduced plasma level of peroxynitrite and the immunohistochemical staining for nitrotyrosine in the ileum and aorta. Our results suggest that during splanchnic artery occlusion shock peroxynitrite formation is likely to be correlated with nitric oxide production from constitutive nitric oxide synthase activation rather than from the inducible isoform enzyme.

Analysis of Variance↗
PubMed2003

Animal and cellular models of chronic pain.

Chronic pain, especially neuropathic pain and cancer pain, is often not adequately treated by currently available analgesics. Animal models provide pivotal systems for preclinical study of pain. This article reviews some of the most widely used or promising new models for chronic pain. Partial spinal ligation, chronic constriction injury, and L5/L6 spinal nerve ligation represent three of the best characterized rodent models of peripheral neuropathy. Recently, several mouse and rat bone cancer pain models have been reported. Primary or permanent cultures of sensory neurons have been established to study the molecular mechanism of pain, especially for neurotransmitter release and signal transduction. The emerging gene microarray, genomics and proteomics methods may be applied to throughly characterize these cells. Each model is uniquely created with distinct mechanisms, it is therefore essential to report and interpret results in the context of a specific model.

Animals↗
PubMed2005

Accessing key steps of human tumor progression in vivo by using an avian embryo model.

Experimental in vivo tumor models are essential for comprehending the dynamic process of human cancer progression, identifying therapeutic targets, and evaluating antitumor drugs. However, current rodent models are limited by high costs, long experimental duration, variability, restricted accessibility to the tumor, and major ethical concerns. To avoid these shortcomings, we investigated whether tumor growth on the chick chorio-allantoic membrane after human glioblastoma cell grafting would replicate characteristics of the human disease. Avascular tumors consistently formed within 2 days, then progressed through vascular endothelial growth factor receptor 2-dependent angiogenesis, associated with hemorrhage, necrosis, and peritumoral edema. Blocking of vascular endothelial growth factor receptor 2 and platelet-derived growth factor receptor signaling pathways by using small-molecule receptor tyrosine kinase inhibitors abrogated tumor development. Gene regulation during the angiogenic switch was analyzed by oligonucleotide microarrays. Defined sample selection for gene profiling permitted identification of regulated genes whose functions are associated mainly with tumor vascularization and growth. Furthermore, expression of known tumor progression genes identified in the screen (IL-6 and cysteine-rich angiogenic inducer 61) as well as potential regulators (lumican and F-box-only 6) follow similar patterns in patient glioma. The model reliably simulates key features of human glioma growth in a few days and thus could considerably increase the speed and efficacy of research on human tumor progression and preclinical drug screening.

Animals↗
PubMed2002

The chronic psychosocial stress paradigm in male tree shrews: evaluation of a novel animal model for depressive disorders.

To improve our knowledge of the causal mechanisms of stress-related disorders such as depression, we need animal models that mirror the situation in patients. One promising model is the chronic psychosocial stress paradigm in male tree shrews, which is based on the territorial behaviour of these animals that can be used to establish naturally occurring challenging situations under experimental control in the laboratory. Co-existence of two males in visual and olfactory contact leads to a stable dominant-subordinate relationship, with subordinates showing distinct stress-induced behavioural and neuroendocrine alterations that are comparable to the symptoms observed during episodes of depression in patients such as constantly elevated circulating glucocorticoid hormones due to a chronic hyperactivity of the hypothalamic-pituitary-adrenal axis. To elucidate whether the chronic psychosocial stress model in tree shrews besides its "face validity" for depression also has "predictive validity", we treated subordinate tree shrews with the tricyclic antidepressant clomipramine and found a time-dependent restoration of both endocrine and behavioural parameters. In contrast, the anxiolytic diazepam was ineffective. Although the chronic psychosocial stress model in tree shrews requires further validation, it has sufficient face, predictive, and construct validity to become an interesting non-rodent model for research on the etiology and pathophysiology of depression.

Animals↗
PubMed2004

Neurogenesis in a rat model of age-related cognitive decline.

Age-related decrements in hippocampal neurogenesis have been suggested as a basis for learning impairment during aging. In the current study, a rodent model of age-related cognitive decline was used to evaluate neurogenesis in relation to hippocampal function. New hippocampal cell survival was assessed approximately 1 month after a series of intraperitoneal injections of 5-bromo-2'-deoxyuridine (BrdU). Correlational analyses between individual measures of BrdU-positive cells and performance on the Morris water maze task provided no indication that this measure of neurogenesis was more preserved in aged rats with intact cognitive abilities. On the contrary, among aged rats, higher numbers of BrdU-positive cells in the granule cell layer were associated with a greater degree of impairment on the learning task. Double-labelling studies confirmed that the majority of the BrdU+ cells were of the neuronal phenotype; the proportion of differentiated neurons was not different across a broad range of cognitive abilities. These data demonstrate that aged rats that maintain cognitive function do so despite pronounced reductions in hippocampal neurogenesis. In addition, these findings suggest the interesting possibility that impaired hippocampal function is associated with greater survival of newly generated hippocampal neurons at advanced ages.

Aging↗
PubMed2000

Animal models in xenotransplantation.

The severe shortage of donor organs has provided a strong impetus to push the investigation into the use of animal organs for humans. Xenotransplantation will not only benefit patients, but also represents a unique and potentially profitable business opportunity. However, there are many barriers to successful clinical xenotransplantation, including immunological barriers, physiological incompatibility, zoonosis and ethical concerns. This overview will focus on currently available animal models used in attempts to break through the immunological barriers to xenotransplantation. There are many advantages to using small animal, namely rodent, models in xenotransplantation research. For example, the use of the mouse model allows the use of knockout mice and careful dissection of rejection mechanisms at the molecular level. The following models can be used to study hyperacute rejection (HAR): guinea-pig-to-rat, mouse-to-rabbit, guinea-pig-to-mouse, rat-to-presensitised mouse and rat-to-alpha-Gal knockout mouse. The hamster-to-rat, mouse-to-rat and rat-to-mouse models are commonly used to study acute vascular rejection. Large animal models are complex and expensive, but they are more relevant to clinical xenotransplantation. Based on experiments using transgenic pig-to-primate models, HAR can be overcome. However, acute vascular rejection remains a major barrier at the present time. A pig cartilage-to-monkey model has been developed to study chronic rejection. Other novel models such as pig venous segment-to-monkey model and rat-to-primate model may represent viable options to study immunological barriers following xenotransplantation. Like many other medical breakthroughs, animal research will continue to make enormous contributions towards the eventual success of xenotransplantation.

Animals↗
PubMed1998

Syngeneic islet transplantation in prediabetic BB-DP rats--a synchronized model for studying beta-cell destruction during the development of IDDM.

During development of IDDM mononuclear cell infiltration is seen in the islets of Langerhans in both man and rodent models. This process is not synchronized in time and space. To create a synchronized model for investigation of the cellular and molecular events during IDDM development, we isolated and transplanted 200 neonatal BB-DP rat islets under the kidney capsule of 30 day old BB-DP rats. Islet transplantations were also carried out from Wistar Furth (WF) to WF rats, from WF to Wistar Kyoto (WK) rats and from WK to BB-DP rats to compare disease occurrence in an islet syngraft with changes in islet syngrafts or allografts in non-diabetes prone recipients and with changes in islet allografts in diabetes prone recipients, respectively. Pancreata and grafts were harvested at pre-scheduled time points before onset of diabetes and at onset of diabetes, and stained for insulin, MHC class I, MHC class II, alphabeta-TCR, CD4, CD8 or ED1. Diabetes incidence in the syngrafted BB-DP rats was 75% at 78 +/- 5 days of age. The incidence and time of onset of IDDM was unaffected by islet syngrafting. Positive correlations were found between the percentage of infiltrated islets in situ and the number of infiltrating cells in the islet syngraft from the same BB-DP rats (p = 0.003-p < 0.0001, r = 0.5-0.7). The number of infiltrating cells regardless of cell type in the graft was inversely correlated to the graft insulin content (p = 0.0003-p < 0.0000, r = -0.6 to -0.8). The graft insulin content was 70% and 90% in BB-DP rats before onset of diabetes and BB-DP rats not developing diabetes respectively, and 30% in the diabetic rats (p < 0.01). Interestingly only 5% of the allografted BB-DP rats developed diabetes. No correlation was found between the number of infiltrating cells in the graft and islets in situ in the BB-DP rats not developing diabetes. Only baseline infiltration was seen in grafts from syngrafted WF rats. In allografted WF islet to WK rats graft rejection was seen 12 days after transplantation. No correlation was found between the number of infiltrating cells in the graft and islets in situ. In conclusion the cellular infiltration in syngeneic but not allogeneic islets grafted to 30 day old BB-rats mirrors that seen in islets in situ. Syngeneic islet grafting in BB-DP rats may be useful for studying the cellular and molecular events during the development of IDDM.

Animals↗
PubMed2005

Helicobacter pylori-infected animal models are extremely suitable for the investigation of gastric carcinogenesis.

Although various animal models have been developed to clarify gastric carcinogenesis, apparent mechanism of gastric cancer was not clarified in recent years. Since the recognition of the pathogenicity of Helicobacter pylori (H pylori), several animal models with H pylori infection have been developed to confirm the association between H pylori and gastric cancer. Nonhuman primate and rodent models were suitable for this study. Japanese monkey model revealed atrophic gastritis and p53 mutation after long-term infection of H pylori. Mongolian gerbil model showed the development of gastric carcinoma with H pylori infection alone, as well as with combination of chemical carcinogens, such as N-methyl-N-nitrosourea and N-methyl-N-nitro-N'-nitrosoguanidine. The histopathological changes of these animal models after H pylori inoculation are closely similar to those in human beings with H pylori infection. Eradication therapy attenuated the development of gastric cancer in H pylori-infected Mongolian gerbil. Although several features of animal models differ from those seen in human beings, these experimental models provide a starting point for further studies to clarify the mechanism of gastric carcinogenesis as a result of H pylori infection and assist the planning of eradication therapy to prevent gastric carcinoma.

Animals↗
PubMed2000

Differential downregulation of GABAA receptor subunits in widespread brain regions in the freeze-lesion model of focal cortical malformations.

Focal cortical malformations comprise a heterogeneous group of disturbances of brain development, commonly associated with drug-resistant epilepsy and/or neuropsychological deficits. Electrophysiological studies on rodent models of cortical malformations demonstrated intrinsic hyperexcitability in the lesion and the structurally intact surround, indicating widespread imbalances of excitation and inhibition. Here, alterations in regional expression of GABA(A) receptor subunits were investigated immunohistochemically in adult rats with focal cortical malformations attributable to neonatal freeze-lesions. These lesions are morphologically characterized by a three- to four-layered cortex with microsulcus formation. Widespread regionally differential reduction of GABA(A) receptor subunits alpha1, alpha2, alpha3, alpha5, and gamma2 was observed. Within the cortical malformation, this downregulation was most prominent for subunits alpha5 and gamma2, whereas medial to the lesion, a significant and even stronger decrease of all subunits was detected. Lateral to the dysplastic cortex, the decrease was most prominent for subunit gamma2 and moderate for subunits alpha1, alpha2, and alpha5, whereas subunit alpha3 was not consistently altered. Interestingly, the downregulation of GABA(A) receptor subunits also involved the ipsilateral hippocampal formation, as well as restricted contralateral neocortical areas, indicating widespread disturbances in the neocortical and hippocampal network. The described pattern of downregulation of GABA(A) receptor subunits allows the conclusion that there is a considerable modulation of subunit composition. Because alterations in subunit composition critically influence the electrophysiological and pharmacological properties of GABA(A) receptors, these alterations might contribute to the widespread hyperexcitability and help to explain pharmacotherapeutic characteristics in epileptic patients.

Animals↗
PubMedDate not supplied

Resistant starch and colorectal neoplasia.

There are several approaches to examining the relationship between resistant starch (RS) and development of colorectal cancer (CRC). These include examination of epidemiological relationships, objective testing of effects of RS given to humans on biological events of relevance to CRC, and studies in animal models where protection and mechanisms of protection can be directly tested. Nine epidemiological studies have examined the relationship between starch and CRC and/or adenomas. Most show a significant protective effect. However, epidemiological tools for measuring consumption of RS are poorly developed and so a benefit for RS can only be inferred. On balance, the magnitude of protection by starch appears to be in the order of 25-50%. Human intervention studies have examined the effect of various types and amounts of RS consumption on colonic biology. To generalize from these studies, RS softens stools and increases stool bulk, decreases pH, increases short-chain fatty acids (SCFAs) including butyrate, reduces products of protein fermentation, and decreases bile salts in fecal water. Such changes seem to be achieved within about 4 weeks of commencing consumption. The greatest effects are seen with the highest doses where increased fecal starch recovery is observed. A modest number of animal studies have been undertaken. Those examining effects of RS on colonic biology and biomarkers for CRC confirm and extend the results in humans. RS modifies the lumenal environment, largely through altered fermentation of polysaccharides and proteins. RS also affects epithelial biology in that it increases apoptotic deletion of genetically damaged cells. More work is needed to define what types and combinations of RS, perhaps with probiotics, exert the greatest effects on colonic environment and epithelial biology, and then to test these in the cancer models for their protective effect. A few studies have examined effect of RS on cancer as an end point in several rodent models, but the results are not clear cut. In conclusion, consumption of RS dramatically affects the colonic lumenal environment and facilitates apoptotic deletion of genetically damaged cells in the colon, several of which are considered to be biomarkers associated with risk for CRC. These effects can be interpreted as reflecting improved colonic health, which might be of benefit in protection against CRC. Direct evidence for protection is still not available.

Animals↗
PubMed2006

Formation of human prostate tissue from embryonic stem cells.

Rodent models and immortalized or genetically modified cell lines are frequently used-but have limited utility-for studying human prostate development and maturation. Using rodent mesenchyme to establish reciprocal mesenchymal-epithelial cell interactions with human embryonic stem cells (hESCs), we generated human prostate tissue expressing prostate-specific antigen (PSA) within 8-12 weeks. This human prostate model shows species-conserved signalling mechanisms that could extend to integumental, gastrointestinal and genital tissues.

Animals↗
PubMed2007

Viral infections as potential triggers of type 1 diabetes.

During the last decades, the incidence of type 1 diabetes (T1D) has increased significantly, reaching percentages of 3% annually worldwide. This increase suggests that besides genetical factors environmental perturbations (including viral infections) are also involved in the pathogenesis of T1D. T1D has been associated with viral infections including enteroviruses, rubella, mumps, rotavirus, parvovirus and cytomegalovirus (CMV). Although correlations between clinical presentation with T1D and the occurrence of a viral infection that precedes the development of overt disease have been recognized, causalities between viruses and the diabetogenic process are still elusive and difficult to prove in humans. The use of experimental animal models is therefore indispensable, and indeed more insight in the mechanism by which viruses can modulate diabetogenesis has been provided by studies in rodent models for T1D such as the biobreeding (BB) rat, nonobese diabetic (NOD) mouse or specific transgenic mouse strains. Data from experimental animals as well as in vitro studies indicate that various viruses are clearly able to modulate the development of T1D via different mechanisms, including direct beta-cell lysis, bystander activation of autoreactive T cells, loss of regulatory T cells and molecular mimicry. Data obtained in rodents and in vitro systems have improved our insight in the possible role of viral infections in the pathogenesis of human T1D. Future studies will hopefully reveal which human viruses are causally involved in the induction of T1D and this knowledge may provide directions on how to deal with viral infections in diabetes-susceptible individuals in order to delay or even prevent the diabetogenic process.

Animals↗
PubMed2000

The Chinese herbal medicine Chai-Hu-Long-Ku-Mu-Li-Tan (TW-001) exerts anticonvulsant effects against different experimental models of seizure in rats.

We evaluated the anticonvulsant effect of Chai-Hu-Long-Ku-Mu-Li-Tan (TW-001), a Chinese herbal medicine, and its mechanisms in several standard rodent models of generalized seizure. TW-001 (4 g/kg, p.o.) significantly increased the threshold for tonic electroconvulsions and the threshold for tonic seizures in response to i.v. infusion of pentylenetetrazole (PTZ). In the s.c. PTZ seizure test, both the incidence and severity of seizures were decreased by TW-001. TW-001 (1-10 mg/ml) did not alter resting membrane potential or input resistance of the hippocampal CA1 neurons, but elicited a reversible suppression of stimulus-triggered epileptiform activity in area CA1 and spontaneously occuring epileptiform burst discharges in area CA3 elicited by picrotoxin. Both field excitatory postsynaptic potentials and population spikes were reversibly depressed by TW-001 (0.5-15 mg/ml) in a concentration-dependent manner. The sensitivity of postsynaptic neurons to a glutamate-receptor agonist, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid or N-methyl-D-aspartate, was not altered by TW-001 (10 mg/ml). However, TW-001 (5 mg/ml) clearly increased the magnitude of paired-pulse facilitation. TW-001 (5-10 mg/ml) reversibly limited the repetitive firing and reduced the maximal rate of rise of action potentials elicited by injection of depolarizing current pulses (0.4 nA, 200 ms) into the pyramidal cells. TW-001 (1-10 mg/ml) exerted a concentration-dependent reduction of the tetrodotoxin-sensitive sodium currents and high voltage-activated calcium currents. These results suggest that TW-001 is an interesting new anticonvulsant agent that exerts its anticonvulsant activity through inhibition of sodium and calcium channels, stabilizing neuronal membrane excitability and inhibiting glutamate release.

Action Potentials↗
PubMed2003

Phylogenetic changes in the expression of delta opioid receptors in spinal cord and dorsal root ganglia.

To assess the validity of rodent models for investigating the role of delta opioid receptors (DOR) in analgesia, the distribution of DOR binding and mRNA were compared between rodent and primate spinal cord and dorsal root ganglia (DRG), using receptor autoradiography and in situ hybridization, respectively. In mouse and rat spinal cord, [(125)I]-deltorphin-labeled DOR binding sites were detected throughout the gray matter. In contrast, in primate and particularly in human spinal cord, DOR binding was mainly present in laminae I-II, with little to no binding in deeper layers. Accordingly, in rodent spinal cord, DOR mRNA was expressed by a large number of neurons distributed throughout the ventral and dorsal horns, whereas in the primate, DOR expression was significantly lower, as evidenced by a moderate number of labeled cells throughout the gray matter in monkey and by only few labeled cells in human, mainly in Clarke's column and lamina IX. Major species differences in DOR expression were also observed in primary afferent cells bodies. In rat DRG, intense DOR mRNA hybridization was primarily observed over large ganglion cells immunopositive for neurofilament 200. In contrast, in monkey and human DRG, DOR mRNA was primarily detected over small and medium-sized ganglion cells. These results demonstrate major differences in the expression and distribution of DOR in the spinal cord and DRG between mammalian species. Specifically, they point to a progressive specialization of DOR toward the regulation of primary somatosensory, namely nociceptive, inputs during phylogeny and suggest that the effects of DOR agonists in rodents may not be entirely predictive of their action in humans.

Animals↗
PubMed2004

Disease-related epitope spread in a humanized T cell receptor transgenic model of multiple sclerosis.

While EAE has been an invaluable model for the immunopathogenesis of multiple sclerosis, it has sometimes been difficult to bridge the gap between findings and therapies in the rodent models and the cellular and molecular interactions that can be studied in the human disease. Humanized transgenic models offer a means of achieving this, through the expression of disease-implicated HLA class II molecules, co-expressed with a cognate HLA-class II-restricted, myelin-specific TCR derived from a human T cell clone implicated in disease. We have generated such a transgenic line, called line 8, that co-expresses a high level of HLA-DR15 and a human TCR specific for HLA-DR15/MBP 85-99. T cells from the transgenic line are skewed to the CD4 single-positive compartment and produce IFN-gamma in response to peptide from mylein basic protein. Mice develop a spontaneous disease phenotype, showing poverty of movement, although this rarely develops into paralysis except following immunization with peptide. On induction of paralysis by immunization with peptide, disease correlates with epitope spread to a number of additional, HLA-DR15-restricted myelin epitopes. This model should be valuable for analyzing epitope spread in a humanized immunogenetic environment and for the testing of specific immunotherapies.

Animals↗
PubMed1999

Androgenetic alopecia: in vivo models.

Androgenetic alopecia is the most common form of balding in humans. There is great interest in finding a reliable animal model to study the pathogenesis and treatment of this abnormality. The sump-tailed macaque (Macaca artoides) has been the standard model and appears to be useful homologue. These primates are reasonably good predictors of compound efficacy. Due to reduced size and expense, rodent models have been sought. Testosterone inducible models require more development but offer potential. Xenografts of human skin to immunodeficient mice, notably nude or severe combined immunodeficiency, are small, relatively inexpensive, and easy to work with if a source of human tissue is available. Xenografts to double mutant mice for severe combined immunodeficiency and a number of hormone receptor null mutations offer new refinements to these xenograft models.

Alopecia↗
PubMed2005

Septations in chronic spinal cord injury cavities contain axons.

Human spinal cord injury (SCI) can result in progressive degeneration that may continue for many years and lead to the formation of highly septated cystic cavities. This hallmark feature has been reproduced in experimental models, but neither its pathogenesis nor clinically relevant features have been fully elucidated. Here, we show for the first time in a rodent model of chronic SCI that the septations spanning cavities contain axons.

Animals↗