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At least 505 records · Page 28Linked to original sources
PubMed2006

Prevention of onset of Parkinson's disease by in vivo gene transfer of human hepatocyte growth factor in rodent model: a model of gene therapy for Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra (SNi). As neurotrophic factors support the survival and enhance the function of dopaminergic neurons, gene therapy using neurotrophic factors has become the center of interest. Thus, we focused on hepatocyte growth factor (HGF) as a neurotrophic and angiogenic growth factor. At 7 days before injection of 6-hydroxydopamine into the SNi, stereotaxic transfection of human HGF or lacZ plasmid was performed into the unilateral striatum of rats. Expression of human HGF in the injected sites could be detected in rats transfected with HGF plasmid DNA, using immunohistochemical staining. Consistently, human immunoreactive HGF protein could be detected at least up to 12 days after transfection. Interestingly, PD rats transfected with lacZ demonstrated amphetamine-induced rotational asymmetry. However, transfection of HGF plasmid DNA resulted in significant inhibition of abnormal rotation up to 24 weeks in a dose-dependent manner. Over 90% of dopaminergic neurons were lost in PD rats transfected with lacZ, whereas over 70% survived in rats transfected with HGF, as assessed by immunohistochemical staining. Overall, the present study demonstrated that overexpression of HGF prevented neuronal death in a PD rat model, providing a potential novel therapy for PD.

Animals↗
PubMed2002

Inhibitors of angiogenesis selectively reduce the malignant cell load in rodent models of human myeloid leukemias.

Angiogenesis is essential for growth and metastasis of solid tumors and probably also for hematological malignancies. Angiogenic inhibitors, like endostatin (ES) and PI-88, retard cancer growth. We tested these in mice with juvenile myelomonocytic leukemia (JMML), and in rats with acute myeloid leukemia (BNML). Eight weeks after transplantation and with a continuous drug treatment for the last 4 weeks, the leukemic cell mass decreased from almost 90% of all bone marrow cells to about 15 and 45% with ES, to about 35 and 55% with PI-88, and to about 10 and 25% with ES + PI-88 in the leukemic mice and rats, respectively. The numbers of normal human bone marrow cells transplanted into mice were unchanged by the treatments. The microvessel density in leukemic animals given ES or PI-88 was 10-50% of that in untreated animals. Notably, simultaneous treatment with ES and PI-88 led to a reduction of about 95% in JMML mice and 85% in BNML rats. In vitro proliferation of either JMML or BNML cells was not significantly altered by either drug, demonstrating the selectivity of ES and PI-88 as angiogenic inhibitors. In conclusion, anti-angiogenic therapy may be a valuable adjunct to conventional treatment of leukemia.

Acute Disease↗
PubMed2004

Methadone maintenance reduces heroin- and cocaine-induced relapse without affecting stress-induced relapse in a rodent model of poly-drug use.

Although it is well established that methadone can be an effective treatment for opiate addiction, it is not clear how methadone maintenance affects cocaine use and cravings in individuals who self-administer both opiates and cocaine. In our attempt to explore the effect of methadone maintenance on the effects of cocaine, we first assessed the locomotor stimulatory effects of cocaine in rats maintained on methadone (0, 10, 20, or 30 mg/kg/day, via osmotic minipumps). Chronic methadone elevated baseline locomotion in a dose-dependent manner and did not reduce the direct stimulatory effects of cocaine (5 mg/kg). We then investigated the effects of the highest methadone maintenance dose (30 mg/kg/day) on heroin and cocaine seeking in extinction, and when it was precipitated by exposure to heroin, cocaine, or foot-shock stress in rats trained to self-administer both drugs in the same experimental context (heroin 0.05 mg/kg/inf; cocaine 0.5 mg/kg/inf, eight 3-h sessions each). In tests of reinstatement, rats responded selectively on the appropriate drug-associated lever after priming injections of heroin (0.25 mg/kg) or cocaine (20 mg/kg). Methadone maintenance blocked both cocaine- and heroin-induced reinstatement, but not stress-induced reinstatement, which was not lever selective. These results suggest that although methadone maintenance may not reduce the direct stimulatory effects of cocaine, it has the potential to reduce both spontaneous and cocaine-primed cocaine-seeking behavior.

Analysis of Variance↗
PubMed1992

Regulation of cardiac adenylate cyclase activity in rodent models of obesity.

We have investigated beta-adrenergic regulation of adenylate cyclase activity in heart tissue membranes from the genetically obese Zucker rat, the genetically obese CBA mouse and the genetically obese diabetic (db/db) mouse. Responsiveness to beta-adrenergic stimulation was impaired in membranes from the obese Zucker rat, but not in the other models. The membranes from obese Zucker rats showed both decreased beta-adrenergic-receptor number and altered coupling between beta-adrenergic receptors and the stimulatory guanine-nucleotide-binding protein, Gs. In contrast, no alterations in either the levels of Gs or the functional interaction between this protein and the catalytic moiety of adenylate cyclase were observed. In these three genetic models of obesity we observe dissimilar alterations in the control of adenylate cyclase.

Adenylyl Cyclases↗
PubMed2002

Bilateral overactivation of the sensorimotor cortex in the unilateral rodent model of Parkinson's disease - a functional magnetic resonance imaging study.

Functional magnetic resonance imaging (fMRI) is used to investigate the basal ganglia (BG)-cortex circuit using a rat model of Parkinson's disease (PD). The model involves a unilateral destruction of the right substantia nigra by intranigral injection of the dopaminergic neurotoxin 6-hydroxydopamine. Volume of cortical activity was measured by the blood oxygenation level-dependent contrast method while applying electrical forepaw stimulation. The main findings are the following. (i) Contrary to the predictions of the classic model but in line with recent experimental results (positron emission tomography, fMRI and electrophysiology), an increased cortical activity in the sensorimotor cortex of PD rats compared with sham-operated or normal rats was found. (ii) A diffuse neuronal activity at large cortical areas that were not related directly to the stimulation used, was observed. (iii) No difference was found between the lesion and the nonlesion hemispheres when the left or the right forepaw was stimulated; both cortices show significant overactivation of the sensorimotor cortices in addition to diffuse cortical activation. The last finding could be explained by either corticocortical connections or by bilateral BG-cortex connections. These finding suggest that the mutual influence of the two hemispheres is important in the pathophysiology of the BG-cortex circuit and might be crucial in predicting treatments.

Animals↗
PubMed2003

Old wine in new bottles: reviving old therapies for alopecia areata using rodent models.

Alopecia areata is regarded as a tissue-restricted autoimmune disease of hair follicles in which follicular activity is arrested because of the continued activity of lymphocytic infiltrates. Actual loss of hair follicles does not occur, even in hairless lesions. A variety of immunomodulating therapies, including contact sensitizers and immunomodulators, are part of the usual armamentarium for this disorder. None of these treatments have been consistent in their efficacy, and many have untoward side effects. Nevertheless, their uses in valid animal models provide a tool to dissect out molecular mechanisms of therapeutic effects. For several decades, both mechlorethamine (for the treatment of cutaneous T cell lymphoma) and anthralin (for the treatment of psoriasis) have been used successfully. When these therapies were tested in rat and mouse alopecia areata models, we found anthralin and mechlorethamine to be the most effective topical modalities, respectively. The underlying cellular mechanisms may act through targeting infiltrative lymphocytes, and the molecular mechanisms may involve specific cytokine expression changes. These visible, accessible, and unilaterally treated animal model systems are ideal for studying novel alopecia areata therapies, particularly in terms of their in vivo molecular mechanisms of action.

Alopecia Areata↗
PubMed2000

Review article: the stages of gastrointestinal carcinogenesis--application of rodent models to human disease.

The development of gastrointestinal cancer in humans and animals occurs through a consecutive series of stages termed initiation, promotion and progression. The characterization of each of these stages has been elucidated in several model systems as well as in human neoplasms. Both single, putatively initiated cells and preneoplastic foci have been identified by marker protein differences as well as by mutational changes. The promotion stage involves the clonal expansion of single initiated cells. Such expansion can be rapidly reversed by a variety of means, of which acute fasting (as exemplified in rat hepatocarcinogenesis) is among the most rapid and efficient. This reversal involves a selective apoptosis of preneoplastic cells and preneoplastic lesions, associated with a marked increase in expression of the proto-oncogene c-myc. Transition of cells from the stage of promotion to that of progression initially involves specific karyotypic alterations, as noted in both the rat liver model and human colon carcinogenesis. In the former, the transition appears to be associated with enhanced expression of the H119 imprinted putative tumour suppressor gene. Thus, the use of model systems may be applied directly to the human circumstance, increasing the potential both for rational prevention of gastrointestinal neoplasia and for new approaches to the therapy of neoplastic disease in the progression stage.

Animals↗
PubMed1999

Characterization of the Kupffer cell response to exogenous endotoxin in a rodent model of obstructive jaundice.

BACKGROUND: Sepsis and endotoxaemia occur frequently in biliary obstruction. Impaired Kupffer cell endocytosis is implicated in these events. Tumour necrosis factor and interleukin 6, secreted by Kupffer cells, are important mediators of sepsis. Kupffer cell clearance of endotoxin and secretion of cytokines in experimental obstructive jaundice were investigated. METHODS: Wistar rats were randomized to bile duct ligation, sham operation or control. Groups (n = 8) were studied 1 and 3 weeks after operation. Kupffer cell function was assessed using in situ hepatic perfusion. RESULTS: Clearance of endotoxin was significantly depressed 1 week (median (interquartile range) 20.3 (10.5-27.1) per cent) and 3 weeks (22.1 (20.2-23.2) per cent) after bile duct ligation compared with that in respective sham animals (35.5 (29.9-41.6) and 40.9 (37.7-47.0) per cent) and controls (39.5 (37.3-46.8) per cent). Secretion of tumour necrosis factor was significantly greater 1 week (1113.7 (706.5-1436. 8) pg/ml) and 3 weeks (1118.2 (775.7-1484.1) pg/ml) following bile duct ligation compared with that in respective sham animals (114.3 (0-178.5) and 107.6 (63.7-166.4) pg/ml) and controls (0 (0-20.7) pg/ml). Interleukin 6 was not secreted by sham or control animals but was present in the perfusate from jaundiced animals at 1 and 3 weeks (52.5 (9.9-89.5) and 66.2 (60.2-193.1) pg/ml). CONCLUSION: These data demonstrate simultaneous impairment of Kupffer cell clearance of endotoxin and increased secretion of proinflammatory cytokines in experimental obstructive jaundice. These diverse responses may contribute to the development of sepsis-related complications in biliary obstruction.

Animals↗
PubMed2002

Maternal and newborn immunization with a human immunodeficiency virus-1 immunogen in a rodent model.

We examined immunization with an inactivated, gp120-depleted human immunodeficiency virus (HIV) antigen in incomplete Freund's adjuvant (IFA), also containing a sequence of immunostimulatory (ISS) DNA, during the last trimester of pregnancy and neonatally in a rat model. Pregnant rats were immunized in the third trimester and their litters were immunized during the newborn period. In addition, litters of rats from non-immunized mothers were immunized during the neonatal period. As another control, pregnant rats were immunized and their litters analysed. Supernants from peripheral blood mononuclear cells (PBMCs) were assayed from newborns at 4 weeks of age for HIV-specific interferon-gamma (IFN-gamma), HIV-specific regulated on activation, normal, T-cell expressed, and secreted (RANTES), and serum for p24 antigen-specific immunoglobulin G (IgG) production. In the animals whose pregnant mothers were immunized and were also immunized during the neonatal period, we observed HIV-specific IFN-gamma production and HIV-specific RANTES production, but weak p24 IgG antibody production. Animals immunized only during the neonatal period developed the highest levels of HIV-specific IFN-gamma production, but somewhat lower levels of HIV-specific RANTES and p24 IgG antibody production. The group of animals whose mothers had received immunizations during the last trimester of pregnancy, but were not immunized during the neonatal period, developed the strongest p24 IgG antibody levels, but little or undetectable HIV-specific IFN-gamma or RANTES production. Neonatal immunization resulted primarily in cell-mediated immune responses, while animals born to mothers who were immunized during the last trimester had primarily an antibody-mediated immune response. Immunization of pregnant animals followed by neonatal immunization resulted in a mixed cell-mediated/antibody type profile in the neonatal animal. Future studies should provide insights into neonatal immunity and potential vaccine approaches to prevent neonatal infection and perinatal transmission.

AIDS Vaccines↗
PubMed2003

Characterization of IgE responses in a rodent model of filariasis and the allergenic potential of filarial antigens using an in vitro assay.

Filarial infections are characterized by high IgE antibody responses. So far, it is not clear whether IgE antibodies are involved in protection, pathology or both. We established a bioassay to detect reactive IgE antibodies in jirds infected with the filaria Acanthocheilonema viteae. Sera of A. viteae-infected jirds were used to sensitize rat basophil leukaemia (RBL) cells and degranulation was stimulated by addition of antigens of A. viteae. Reactive IgE responses were detected from 2 weeks post infection (p.i.) and throughout the A. viteae infection. Male antigen triggered the strongest mediator release, followed by female worms, infective larvae (L3) and microfilariae. Separation of male and female antigen indicated that several antigens of both genders are potent allergens. In particular, one male specific allergen of about 550 kDa induced strongest degranulation of RBL cells. In addition, mediator release stimulated by antigen fractions of about 15 kDa was due to filarial cystatin. In conclusion, we describe a convenient in vitro assay to examine IgE mediated responses in jirds. A sex specific filarial protein with high allergenic potential is identified and cystatin is established as a potent allergen of A. viteae.

Allergens↗
PubMed2003

Effect of haemodilution with diaspirin cross-linked haemoglobin on the oxygen reserve in a rodent model of surgical blood loss.

The efficacy of pre-operative haemodilution is limited by the reduction in haemoglobin concentration. Acellular haemoglobin-based oxygen carriers provide an alternative to colloid as a haemodiluent, potentially extending the safe limits of this procedure. The aim of this investigation was to determine whether haemodilution with a cross-linked haemoglobin solution, diaspirin cross-linked haemoglobin solution (DCLHb), would enhance the oxygen reserve compared to pentastarch. Sprague Dawley rats were placed in a metabolic box to directly measure systemic oxygen consumption (VO2). Rats were randomized to be haemodiluted to a cellular haemoglobin of 80 g L(-1) with either DCLHb or pentastarch. Oxygen reserve was assessed during isovolemic haemorrhage by determining the critical oxygen delivery (DO2crit) and haemoglobin concentration at the point of oxygen supply dependency (OSD). Following haemodilution and for the duration of the experiment, cardiac index (CI) was significantly lower and systemic vascular resistance was significantly higher in the DCLHb than the pentastarch group. The DO2crit (3.2 +/- 0.4 mL minAg(-1) and 3.4 +/- 0.5 mL minAg(-1), DCLHb versus pentastarch) and cellular haemoglobin concentration (51 +/- 9 g L(-1) and 48 +/- 9 g L(-1)), at which rats entered OSD were similar in both groups. Total haemoglobin concentration (cellular and plasma DCLHb) and arterial oxygen content were significantly higher in the DCLHb group (total haemoglobin, 66 +/- 8 g L(-1) and arterial content, 9.2 +/- 1.4 mL dL(-1)) compared to the pentastarch group (total haemoglobin, 48 +/- 9 g L(-1) and arterial content, 7.3 +/- 1.4 mL dL(-1)). Oxygen extraction ratios increased from baseline levels to 0.53 +/- 0.07 and 0.56 +/- 0.1, for the DCLHb and pentastarch groups, respectively, and were not significantly different. The increase in arterial oxygen content from DCLHb in plasma was offset by the decrease in CI observed in this group. Plasma DCLHb did not extend the limits of haemodilution beyond the capacity of the cellular haemoglobin concentration.

Animals↗
PubMed1997

Trypanocidal effect of Ir-(COD)-pentamidine tetraphenylborate on Trypanosoma brucei and T. b. gambiense rodent models and serum kinetics in sheep.

Pentamidine di-(iridium cyclo-octadiene)tetraphenylborate, called Ir-(COD)-pentamidine tetraphenylborate, was selected from a primary screening as a promising trypanocidal compound. The compound was evaluated against three isolates: Trypanosoma brucei brucei CMP, T.b. brucei GVR 35 and T.b. gambiense Feo. On the T.b. brucei GVR 35 murine CNS model, no mouse was cured when the treatment was commenced 21 days post-infection whatever the treatment regimen. Nevertheless, in vitro the compound killed the trypomastigote forms of T. b. gambiense Feo at 0.6 microM. In vivo, the compound cured all mice infected 1 hour previously with T. b. gambiense Feo after a 10 mg/kg (6.3 mumol/kg) treatment subcutaneously administered in a single dose. Moreover, the compound was active at 1 mg/kg (0.6 mumol/kg) in a single dose against the early stage of the T. b. brucei Antat 1-9 sheep model. Serum kinetics data showed that pentamidine di-(iridium cyclo-octadiene) tetraphenylborate was distributed within deep compartment according to a monocompartmental model. The maximum iridium serum concentration was 198 micrograms/l corresponding to 1 mumol/kg of iridium derivative and this value remained stable for 30-50 hours post-treatment. Iridium was completely eliminated from the serum 700 hours post-treatment. all data obtained from these models are in favour of an activity in the early stage of the disease but indicate that the compound could not cross the blood-brain barrier despite its lipophilicity. Although iterative treatments with the compound rapidly induced the selection of iridium derivative refractory populations, the compound could be studied on pentamidine refractory strains.

Animals↗
PubMed1998

Characterization of perforant path lesions in rodent models of memory and attention.

Early stage Alzheimer's disease (AD) pathology is associated with neurodegeneration of systems within the temporal cortex, e.g. the entorhinal cortex, perforant pathway and hippocampus. The perforant pathway provides the major neuronal input to the hippocampus from the entorhinal cortex and thus relays multimodal sensory information derived from cortical zones into the hippocampus. The earliest symptoms of AD include cognitive impairments, e.g. deficits in short-term memory and attention. Consequently, we have investigated the effect of bilateral knife cut lesions to the perforant path on cognition in rats using models measuring primarily short-term memory (operant delayed match to position task), attention (serial five-choice reaction time task) and spatial learning (Morris water maze). Rats receiving bilateral perforant path lesions showed normal neurological function and a mild hyperactivity. The lesion produced little effect on attention assessed using the five-choice task. In contrast, animals with equivalent lesions showed a robust delay-dependent deficit in the delayed match to position task. Spatial learning in the water maze task was also severely impaired. The delay-dependent deficit in the match to position task was not reversed by tacrine (3 mg/kg) pretreatment. The present data support a selective impairment of cognitive function following perforant path lesions that was confined to mnemonic rather than attentional processing. These findings complement primate and human studies identifying a critical role of the perforant pathway and associated temporal lobe structures in declarative memory. Degeneration of the perforant pathway is likely to contribute to the mnemonic deficits characteristic of early AD. The failure of tacrine to ameliorate these deficits may be relevant to an emerging clinical literature suggesting that cholinomimetic therapies improve attentional rather than mnemonic function in AD.

Animals↗
PubMed2000

Brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 prevent the death of striatal projection neurons in a rodent model of Huntington's disease.

Intrastriatal injection of quinolinate has been proven to be a very useful animal model to study the pathogenesis and treatment of Huntington's disease. To determine whether growth factors of the neurotrophin family are able to prevent the degeneration of striatal projection neurons, cell lines expressing brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), or neurotrophin-4/5 (NT-4/5) were grafted in the adult rat striatum before quinolinate injection. Three days after lesioning, ongoing cell death was assessed by in situ detection of DNA fragmentation. In animals grafted with the control cell line, quinolinate injection induced a gradual cell loss that was differentially prevented by intrastriatal grafting of BDNF-, NT-3-, or NT-415-secreting cells. Seven days after lesioning, we characterized striatal projection neurons that were protected by neurotrophins. Quinolinate injection, alone or in combination with the control cell line, induced a selective loss of striatal projection neurons. Grafting of a BDNF-secreting cell line pre-vented the loss of all types of striatal projection neurons analyzed. Glutamic acid decarboxylase 67-, preproenkephalin-, and preprotachykinin A- but not prodynorphin-expressing neurons were protected by grafting of NT-3- or NT-4/5-secreting cells but with less efficiency than the BDNF-secreting cells. Our findings show that neurotrophins are able to promote the survival of striatal projection neurons in vivo and suggest that BDNF might be beneficial for the treatment of striatonigral degenerative disorders, including Huntington's disease.

Animals↗
PubMed2001

Effect of prophylactic transfusion of stored RBCs on oxygen reserve in response to acute isovolemic hemorrhage in a rodent model.

BACKGROUND: The storage of RBCs results in a time-related decline in 2,3 DPG that may reduce the ability to unload oxygen (O(2)) to tissue. The objective of this study was to compare the effect that transfusion of stored 2,3 DPG-depleted rat blood (7 days in CPDA-1) had on the O(2) reserve in conscious rats, with that of the transfusion of fresh blood (<2-hour storage). STUDY DESIGN AND METHODS: Anemic rats (Hb, 80 g/L) received either fresh packed RBCs or stored RBCs to raise Hb levels to 140 g per L. They then underwent isovolemic hemorrhage mimicking surgical blood loss to the point of O(2) supply dependency (OSD). Critical O(2) delivery (DO(2)crit), Hb concentration, and O(2) extraction at OSD were measured in a metabolic chamber. RESULTS: After transfusion, RBC DPG decreased by 50 percent in the stored-blood group, and the p50 value decreased by 5 mmHg (32.1 +/- 2.5 mmHg vs. 37.5 +/- 3.0). DO(2)crit was similar in the two groups (fresh blood: 2.79 +/- 0.44 mL/min x g(-1); stored blood, 2.99 +/- 0.76 mL/min x g(-1)). The critical Hb concentration at DO(2)crit was higher in the stored-blood group (44 +/- 4 g/L) than in the fresh-blood group (38 +/- 5 g/L); the cardiac index and O(2) extraction ratio in the two groups were not different. Under conditions of severe normovolemic anemia in rats, depletion of DPG and a decrease in p50 had only minor effects on the O(2) reserve. At OSD, under these conditions, O(2) consumption is not limited by diffusion. CONCLUSION: The physiologic impact of DPG depletion in transfused stored blood on oxygen availability in normal rats appears to be small and may be clinically inconsequential.

Anemia↗
PubMed2000

Treatment of inflammatory bowel disease in a rodent model with the intestinal growth factor glucagon-like peptide-2.

BACKGROUND/PURPOSE: Microinjection of a Fisher (F344) rat zygote with human HLA-B27 and beta2-microglobulin genes induces spontaneous chronic gastrointestinal (GI) inflammation similar to lesions seen in patients with inflammatory bowel disease (IBD). This study was designed to evaluate the potential therapeutic benefit of GLP-2, an intestinal growth factor, in this transgenic rat model of IBD. METHODS: Five F344 (control) and 10 HLA-B27 (on a F344 background) rats at 25 weeks of age were used. Rats were divided into the following 3 groups: group 1, F344 rats, no treatment (n = 5); group 2, HLA-B27, no treatment (n = 5); and group 3, HLA-B27, treated with a 14-day systemic infusion (via the jugular vein) of GLP-2 at 50 microg/kg/d (n = 5). After infusion, all rats underwent laparotomy, and the intestine from the ligament of Treitz to the rectum was harvested. Total mucosal damage (percent surface area) was measured using image analysis software (Sigmascan 2.0). Microscopic analysis was performed by a blinded reviewer and scored as follows: 0, no inflammation; 1, mild inflammation; 2, moderate inflammation; and 3, severe inflammation. Colonic mucosal total RNA was assayed for tumor necrosis factor alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-2 (IL-2), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), internal standard, mRNA by reverse transcriptase polymerase chain reaction. Statistical analysis was performed using analysis of variance (ANOVA) and expressed as mean +/- SEM. RESULTS: Normal F344 rats did not show evidence of gross or histological lesions in the small or large intestine. GLP-2 reduced total mucosal damage from 9.0% +/- 0.7% in group 2 to 0.9% +/- 0.5% in group 3 (P < .01). The histological lesion score was reduced from 7.0 +/- 0.6 in group 2 to 4.4 +/- 0.8 in group 3 (P < .01). Furthermore, GLP-2 reduced the mean band intensity (MBI) of TNF-alpha (0.4 +/- 0.04 in group 2 to 0 in group 3, P < .01) and IFN-gamma (0.3 +/- 0.02 in group 2 to 0 in group 3, P < .01). CONCLUSIONS: These data show for the first time that GLP-2 significantly reduces gross (90% decrease) and histological (40% decrease) lesions in this rat model of IBD. This is further supported by a significant decrease in gene expression of the inflammatory mediators TNF-alpha (100% decrease) and IFN-gamma (100% decrease). These data suggest a potential therapeutic role for GLP-2 in IBD.

Animals↗