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PubMed2005

Effect of antibacterial cathelicidin peptide CAP18/LL-37 on sepsis in neonatal rats.

Cathelicidins are a family of antibacterial peptides. Human cathelicidin LL-37 inhibits the binding of endotoxin lipopolysaccharide (LPS) to CD14-positive cells and could ameliorate sepsis. The aim of this study was to observe the effect of LL-37 on sepsis in neonatal rats. Intraperitoneal injection (IPI) of LPS was used to create sepsis in suckling rats. Group 1 rats were given LPS with LL-37, group 2 rats were given LL-37 2 h after LPS, and group 3 rats were given LPS without LL-37. Control group rats were given isovolemic normal saline by IPI. Rats given LL-37 IPI were divided into seven subgroups. Following IPI, an overall assessment score (OAS) and rectal temperature (RT) were assessed hourly. Serum C-reactive protein (CRP) was also assessed at death or at sacrifice 10 h after IPI. All rats in group 3 died. For rats receiving lower doses of LL-37 in groups 1 and 2, mortality was decreased. No deaths occurred among those receiving higher doses of LL-37 in group 1; however, mortality increased in group 2. In group 1, OAS and RT deteriorated initially for those receiving lower doses of LL-37, then improved. OAS and RT did not deteriorate throughout the study in rats given higher doses of LL-37. In group 2 rats given higher doses of LL-37, OAS and RT were not significantly different from rats in group 3. CRP was significantly decreased in group 1 compared with group 3, and decreased in group 2 for lower doses only. We conclude that LL-37 may prevent sepsis and be useful in lower doses for treating sepsis. However, LL-37 appears to have adverse effects when used at higher doses for treating sepsis.

Animals↗
PubMed2003

Short-term dietary conjugated linoleic acid supplementation does not enhance the recovery of immunodepleted dexamethasone-treated rats.

BACKGROUND: Conjugated linoleic acid (CLA) has been reported to decrease fat deposition, and increase lean body mass. This has been broadly inferred to mean that CLA alters protein turnover. However, data to test the effects of CLA on protein turnover are lacking. An enhancement in immune responses by CLA has also been demonstrated. AIM OF THE STUDY: The objective of this study was to determine the potential for dietary CLA and protein intervention to improve nutritional and functional recovery in an animal model of catabolic stress and immunodepletion. METHODS: Diets varying in their protein levels in the presence or absence of CLA were tested for their effects on the recovery of glucocorticoid (intraperitoneal injection of dexamethasone, 120 mg/kg) treated rats. Following steroid injection, rats were fed 4 dietary treatments for 4 d. The diets contained 10 or 20 g/100 g protein with or without 0.5 g/100 g CLA. RESULTS: Dexamethasone treatment resulted in a decreased food intake and loss of weight, independent of dietary treatment. A higher number of blood monocytes occurred in rats fed the high CLA diets. The protein fractional synthesis rate in spleens of rats fed the diets containing either high proteins or CLA were higher compared to those fed diets with low protein content or without CLA, respectively. CLA, consumed post-dexamethasone treatment, did not improve protein turnover in the other tissues studied, including gut mucosa, liver, muscle and thymus. CONCLUSIONS: The present study was performed to determine the effect of CLA in acute conditions, as opposed to a preventive approach, on the recovery from a catabolic stress with immunodepletion. Overall, no effect of short-term feeding CLA on the recovery from dexamethasone-mediated immunodepletion was observed.

Animals↗
PubMed2004

Low-dose anesthesia for corneal transplantation in mice.

BACKGROUND: Despite technical difficulties caused by the small dimensions, scientific and economic considerations stimulated activities in the murine keratoplasty model. Delicate surgery requires stable anesthesia with rapid postoperative waking. METHODS: For corneal transplantation, all animals were intraperitoneally injected with 0.08 ml of a 1:8 mixture of 2% xylazine and 2.5% esketamine hydrochloride. Thus they all received 0.18 mg of xylazine and 1.8 mg of ketamine. In other words, 4.5 mg/kg BW of xylazine and 45 mg/kg BW of ketamine were injected in a mouse weighing 25 g. The inhalation anesthetic isoflurane was used for short interventions like removing lid sutures or in the case of an animal awaking before the end of the operation. A small but effective set of apparatus comprising a glass bottle, a test tube and several interconnected syringes was developed to create a closed system and visualize the amount of isoflurane used in the animal. Air bubbles showed the amount of isoflurane escaping from the opened respiratory mask. RESULTS: The dose reduction of systemic anesthesia requires additional inhalation anesthesia with isoflurane in nearly all cases. The equipment developed is easy to handle and allows systemic anesthesia with a very low dose. CONCLUSION: This murine anesthesia model may be expected to help other surgeons performing corneal transplantations in mice.

Anesthesia, General↗
PubMed2004

Effect of bicarbonate on retinal vasculature and acidosis-induced retinopathy in the neonatal rat.

BACKGROUND: Systemic acidosis induces preretinal neovascularization (NV) analogous to retinopathy of prematurity (ROP) in the neonatal rat. Sodium bicarbonate is used in human neonates to treat acidosis. The effects of alkali administration on the developing retinal vasculature and on acidosis-induced retinopathy (AIR) are unknown. We investigated the effect of sodium bicarbonate gavage on the retinal vasculature of normal and acidotic neonatal rats to determine (1) whether bicarbonate treatment is associated with preretinal NV and (2) whether AIR can be prevented with systemic bicarbonate treatment. METHODS: The extent of acidosis and alkalosis were initially determined from carotid arterial blood samples. In the bicarbonate-alone study, newborn rats were randomized into litters of 25 and received bicarbonate doses of 15 mmol/kg twice daily and 20 mmol/kg once daily from days 2 to 7. Control animals received saline gavage. In the AIR treatment study, acidosis was induced in neonatal rats by intraperitoneal injection of acetazolamide 200 mg/kg from days 2 to 7. Acetazolamide-treated rats received either additional bicarbonate gavage or no additional treatment. Eyes were enucleated on day 13, and the retinal vasculature was assessed for NV using ADPase staining techniques and light microscopy. RESULTS: Systemic alkalosis (peak pH 7.55+/-0.02; mean +/- SD) was confirmed with bicarbonate gavage, and partial reversal of acidosis was confirmed when acetazolamide-treated rats received bicarbonate. Surviving rats receiving bicarbonate 15 mmol/kg twice daily (28% survival) and 20 mmol/kg bicarbonate once daily (45% survival) had an incidence of preretinal NV of 9% and 8%, respectively. No NV was seen in saline-control rats. In the acetazolamide-treated rats, the incidence of preretinal NV in surviving rats was numerically lower in bicarbonate-treated rats than acetazolamide-only controls (8% versus 24%, p=0.065) but with only 19% survival in the bicarbonate-treated rats. CONCLUSIONS: In the neonatal rat, alkalosis induced by bicarbonate gavage is associated with a low incidence of mild, preretinal NV similar to ROP. Although treating acidotic rats with bicarbonate may reduce the incidence of preretinal NV, treatment was associated with an unacceptable mortality rate.

Acetazolamide↗
PubMed1998

Retinal degeneration induced by N-methyl-N-nitrosourea in Syrian golden hamsters.

BACKGROUND: The sequential retinal changes in Syrian golden hamsters induced by N-methyl-N-nitrosourea (MNU) have not been studied. METHODS: Female hamsters received a single intraperitoneal injection of 90 mg/kg MNU at 50 days of age, and the retina was examined light and electron microscopically, immunohistochemically and by the TdT-mediated dUTP-digoxigenin nick end labeling (TUNEL) method until 20 weeks after the treatment. RESULTS: The retinal changes were as follows: (1) Photoreceptor apoptosis occurred 1 day after the treatment and resulted in photoreceptor loss at day 7. During the degeneration, Müller cell proliferation was conspicuous at day 5. (2) After the photoreceptor cell loss, migration of the pigment epithelial cells in all layers of the retina which were in contact with blood vessels occurred. Due to the Müller cell proliferation, gliosis was prominent at the later stage. CONCLUSIONS: The MNU injection caused photoreceptor apoptosis followed by pigment epithelial cell migration around the blood vessels, accompanied by gliosis. The primary event and the course of this disease closely resemble those of retinitis pigmentosa in humans.

Animals↗
PubMed2002

Immunohistochemical studies on the expression pattern of molecular chaperones HSC70 and HSP25 and cell cycle-related proteins cyclin D1 and PCNA in rat liver after thioacetamide intoxication.

Intoxication of rats with thioacetamide (TAA) is a model system to investigate mechanisms involved in liver cell death and tissue reconstitution. Our study was undertaken to determine by immunohistochemistry the expression pattern of the cytoprotective chaperone proteins HSC70 and HSP25 and proliferation markers cyclin D1 and PCNA in livers of Wistar rats intraperitoneally injected with TAA at a single dose of 50 mg/kg. For each protein studied we observed distinct dynamic changes in appearance and localization in liver lobules. During 24-36 h after TAA injection the HSC70 cytoplasmic immunoreaction gradually disappeared from hepatocytes localized around central veins and a shift of immunostaining to cell nuclei took place. Then, 36-48 h after TAA injection the HSC70 cytoplasmic immunoreaction reappeared with the highest intensity in hepatocytes surrounding the areas of inflammatory cells. HSP25, undetectable in control hepatocytes began to appear at approximately 36 h after TAA injection and HSP25-immunopositive cells formed a characteristic ring around areas of inflammation. Of the proteins studied, the most rapid reaction to TAA was observed for cyclin D1. As early as 15 min after TAA administration cyclin D1-positive hepatocytes appeared in intermediate and periportal areas of liver lobules and a subsequent shift of staining to centrilobular hepatocytes took place at 36 and 48 h. There was no correlation of cyclin D1 localization either with PCNA-positive cells or mitotic cells. Our observations suggest that in TAA-treated livers HSP25 and HSC70 proteins can play an anti-inflammatory role, and the early and distinct cyclin D1 expression is not related to proliferation of hepatocytes.

Animals↗
PubMed2002

Enhancement of immunoreactivity for endothelin-1 and endothelin-converting enzyme-1 in the cadmium-treated rat thoracic aorta.

Male rats received daily intraperitoneal injections of cadmium sulfate (2.0 mg/kg) for 3, 6, and 8 days (cadmium-treated groups) or physiological saline for 8 days (control group). The thoracic aortae from both groups were used for electron microscopy and immunocytochemistry for big endothelin (ET)-1, ET-1 and ET-converting enzyme (ECE)-1, and the blood plasma and homogenized thoracic aortae were prepared for assays of big ET-1 and ET-1 concentrations. A remarkable increase in the number of Weibel-Palade (WP) bodies, enhanced immunoreactivities for ET-1 and ECE-1 along the endothelium, and elevated concentrations of ET-1 in the blood plasma as well as in homogenized thoracic aortae were observed in the cadmium-treated groups. However, immunoreactivity for big ET-1 and the plasma and aortic tissue concentrations of big ET-1 did not show any significant changes between the control and cadmium-treated groups. By immunoelectron microscopy, immunoreactivities for ET-1 and ECE-1 were much more pronounced in the increased WP bodies. Since WP bodies are involved in the extracellular release of ET-1 in the manner of a regulated pathway, these findings indicate that cadmium administration induces the enhanced release of ET-1, which is actively processed by ECE-1 in the WP bodies.

Animals↗
PubMed1998

Behaviour of spermatogonia following recovery from busulfan treatment in the rat.

This study describes the morphological behaviour of spermatogonia following recovery from two doses of busulfan treatment in the rat. Twenty days after the second intraperitoneal injection of busulfan, the testes lost most of their spermatogenic cells and there were fewer dispersed singly surviving spermatogonia. These surviving cells were in close contact with the basal portions of adjacent Sertoli cells and the shrunken basal lamina, and were the source for repopulating the depleted seminiferous epithelium. During the initial stage of repopulation (48 days later), surviving spermatogonia underwent a phase of active proliferation: type A spermatogonia underwent symmetric and asymmetric divisions; type B spermatogonia underwent asynchronous differentiation. At day 96, normal spermatogenesis was fully recovered in many seminiferous tubules, represented by 80% of the rats regaining various degrees of fertility at day 120. These data provide an additional model for the study of self-renewal of stem spermatogonia and suggest that the asymmetric division of type A spermatogonia and their close contact with both the basal lamina and the Sertoli cells may be involved in regulating the number of stem spermatogonia and the delicate process of normal spermatogenesis.

Animals↗
PubMed2001

Pineal indoles stimulate the gene expression of immunomodulating cytokines.

Male C57 mice received 10 consecutive daily intraperitoneal injections of melatonin, 5-methoxytryptamine or 5-methoxytryptophol (5mg/kg body weight). Control mice received the alcoholic saline vehicle. All mice were sacrificed 24 hours after the last injection. Following extraction of RNA from peritoneal exudate cells (PEC) and splenocytes, the level of gene expression was analyzed with the reverse transcription-polymerase chain reaction (RT-PCR). The results revealed that melatonin up-regulated the level of gene expression of transforming growth factor-beta (TGF-beta), macrophage-colony stimulating factor (M-CSF), tumor necrosis factor-alpha (TNF-alpha) and stem cell factor (SCF) in PEC, and the level of gene expression of interleukin-1beta (IL-1beta), M-CSF, TNF-alpha, interferon-gamma (IFN-gamma) and SCF in splenocytes. 5-Methoxytryptamine augmented the level of gene expression of TGF-beta, M-CSF and SCF in PEC, and the level of gene expression of IL-1beta, TNF-alpha, IFN-gamma, M-CSF and SCF in splenocytes. 5-Methoxytryptophol elevated the level of gene expression of TNF-alpha, IL-1beta, TGF-beta and M-CSF in PEC, and the level of gene expression of inducible nitric oxide synthase (iNOS), IL-1beta, M-CSF, TNF-alpha, IFN-gamma and SCF in splenocytes.

5-Methoxytryptamine↗
PubMed2005

The antioxidant effect of beta-Glucan on oxidative stress status in experimental spinal cord injury in rats.

This study was performed to investigate the antioxidant effect of beta-Glucan in experimental spinal cord injury (SCI). Injury was produced using weight-drop technique in rats. beta-Glucan was given by intraperitoneal injection following trauma. The rats were sacrificed at the sixth day of injury. Oxidative stress status was assessed by measuring the spinal cord tissue content of Malonyldialdehyde (MDA), Superoxide Dismutase (SOD) and Gluthatione Peroxidase (GSH-Px) activities. No effect of beta-Glucan on SOD and MDA activities was found but, GSH-Px levels were found to decrease to the baseline (preinjury) levels when it was compared to untreated group (U=0.000; p=0.002). According to our results, beta-Glucan works like a scavenger and has an antioxidant effect on lipid peroxidation in spinal cord injury.

Animals↗
PubMed2004

Radioprotection of the murine submandibular gland by isoproterenol: autoradiography study with 3H-leucine.

Irradiation of the salivary glands results in the generation of free radicals from metal ions present in the secretory granules of acinar cells, a process that is believed to exacerbate radiation damage to the salivary glands. We therefore conducted a comparative investigation of radiation damage to the acinar cells of murine submaxillary glands in which granule secretion had been induced, and used autoradiography to visualize the pathological changes. Male BALB/c mice, at 8 weeks of age, were divided into four groups: a no-isoproterenol (IPR) and no-irradiation group (group I), a no-IPR, irradiated group (group II), an IPR, no-irradiation group (group III), and an IPR, irradiated group (group IV). Intraperitoneal injections of IPR were used, and 3 h later, the submaxillary region was irradiated with X-rays at a dose of 10 Gy. Three days after the irradiation, 3H-leucine was administered, and submaxillary glands were removed at predetermined times. Thin sections were prepared, and light- and electron-microscope autoradiography was performed. The number of reduced silver particles per unit acinar cell area was determined by light-microscopic autoradiography, and the proportion of reduced silver particles in the rough endoplasmic reticulum, the Golgi apparatus, and secretion granules was determined by electron-microscopic autoradiography. The result indicated that the effects of the radiation on the secretory potential of the submaxillary glands were diminished in acinar cells with a higher secretory granule content.

Adrenergic beta-Agonists↗
PubMed2004

Intraperitoneal administration of adenosine inhibits formation of abdominal adhesions.

PURPOSE: Previously we demonstrated that peritoneal lavage with high concentrations of adenosine (1 mM) provides pharmacologic levels of adenosine in the intestines without elevating adenosine levels in the systemic circulation and without causing systemic hemodynamic effects (Alimentary Pharmacology & Therapeutics 2000; 14:1371-80). Because adenosine can be safely administered into the peritoneal cavity, and because it inhibits fibroblast proliferation and collagen production and inflammation and enhances angiogenesis, we tested the hypothesis that adenosine applied into the abdominal cavity safely and effectively reduces formation of abdominal adhesions. METHODS: To test this hypothesis, in Sprague-Dawley rats, a window of right parietal peritoneum was removed and the cecum was brushed and placed next to the damaged peritoneum. After injury, rats received in the abdominal cavity either 20 ml of saline (n = 12, Saline Group) or 20 ml of 1 mM adenosine (n = 12, Adenosine 1X Group; and n = 12, Adenosine 4X Group). At 24, 48, and 72 hours after surgery, rats received by intraperitoneal injection either 10 ml of saline (Saline Group and Adenosine 1X Group) or 10 ml of 1 mM adenosine (Adenosine 4X Group). RESULTS: After 14 days, the degree of adhesion formation was scored (0 to 4) by a blinded observer. Animals tolerated the adenosine treatments without signs of discomfort or distress. The adhesion scores were 2.6 +/- 0.34, 1.7 +/- 0.40, and 0.74 +/- 0.29 in the Saline, Adenosine 1X, and Adenosine 4X groups, respectively (P = 0.0035, Kruskal-Wallis analysis of variance). CONCLUSION: Peritoneal administration of 1 mM adenosine safely and effectively reduces adhesion formation.

Adenosine↗
PubMed2006

Effects of semax against the background of dopaminergic receptor blockade with haloperidol.

We studied the neurotropic effects of ACTH(4-10) analog semax against the background of dopaminergic receptors blockade with haloperidol. Intranasal administration of semax (0.05, 0.2, and 0.6 mg/kg) produced virtually no effect on disturbances of orientation and exploratory reactions and motor activity caused by intraperitoneal injection of 0.2 mg/kg haloperidol. By contrast, preliminary administration of 0.05 mg/kg semax prevented haloperidol-induced disturbances in active avoidance conditioning.

Administration, Intranasal↗
PubMed2006

Effects of L-arginine on various types of pain sensitivity.

Intraperitoneal injection of L-arginine to male Wistar rats 12 min before the start of the experiment produced a nociceptive effect on models of electrocutaneous stimulation of the tail or hot-plate test and increased nociceptive behavior due to high sensitivity of supraspinal nociceptive structures to this compound. The nociceptive effect of this amino acid was more pronounced and persistent under conditions of electrocutaneous stimulation.

Animals↗
PubMed2005

Systemic iron supplementation replenishes iron stores without enhancing colon carcinogenesis in murine models of ulcerative colitis: comparison with iron-enriched diet.

Ulcerative colitis (UC) patients frequently require iron supplementation to remedy anemia. The impact of systemic iron supplementation (intraperitoneal injection) on UC-associated carcinogenesis was assessed in mice subjected to cyclic dextran sulfate sodium (DSS) treatment and compared with dietary iron enrichment. Systemic iron supplementation, but not a twofold iron diet, remedied iron deficiency as indicated by the histochemical detection of splenic iron stores. A twofold iron diet, but not systemic iron, increased iron accumulation in colonic luminal contents, at the colonic mucosal surface, and in superficial epithelial cells. Colitis-associated colorectal tumor incidence after 15 DSS cycles was not affected by systemic iron (2/28; 7.1%) compared to nonsupplemented controls (4/28; 14.1%) but was significantly increased by the twofold iron diet (24/33; 72.7%) (P < 0.001). Mechanistic study revealed that systemic iron had no effect on DSS-induced inflammation, or colonic iNOS and COX-2 protein levels, compared to controls. Systemic iron supplementation for 16 weeks replenished splenic iron in a spontaneous colitis model (interleukin-2-deficient mice) and significantly reduced colonic inflammation compared to interleukin-2 (-/-) controls without increasing hyperplastic lesions. These results suggest that iron supplemented systemically could be used to remedy anemia in UC patients without exacerbating inflammation or enhancing colon cancer risk. These findings need to be verified in clinical studies.

Adenocarcinoma↗
PubMed2006

Pharmacological activity of ruthenium complexes trans-[RuCl(2)(L)4] (l = nicotinic or i-nicotinic acid) on anxiety and memory in rats.

Many biological properties have been attributed to ruthenium complex I (trans-[RuCl(2)(nic)(4)]) and ruthenium complex II (trans-[RuCl(2 )(i-nic)( 4)]) including nitric oxide synthase inhibition. In this study, we evaluated pharmacological effects of these complexes on anxiety and memory formation. Memory was evaluated with inhibitory avoidance and habituation to an open-field and anxiety was tested with elevated plus-maze. Adult male Wistar rats (250 to 350 g) received intraperitoneal injections of vehicle, ruthenium complex I (45.2, 90.4, or 180.7 mumol/kg), or ruthenium complex II (0.08, 4.5, or 13.6 mumol/kg) 30 min prior open-field training or elevated plus-maze test and 30 min or 0 h after training. No effects were observed in the anxiety parameters and habituation to an open-field. The ruthenium complexes impaired memory retention compared with vehicle group in the inhibitory avoidance, as when administrated 30 min prior as immediately after training. The memory impairment induced by ruthenium complexes may be due to their nitric oxide synthase inhibition capacity.

Animals↗
PubMed2004

C-fiber activation exacerbates sleep-disordered breathing in rats.

We reported previously that activation of vagal feedback by protoveratrines or serotonin exacerbates sleep apnea in rats, but each of these agents activates multiple afferent fiber types. To elucidate the specific impact of C-fiber activity on sleep apnea, the present study utilized capsaicin (CAP), which stimulates C-fibers via the CAP receptor. Nine adult Sprague-Dawley rats were instrumented for chronic polysomnography and recorded for 6 hours on four occasions. Prior to each recording, the animals received an intraperitoneal injection of either saline (control), or CAP 0.1, 1.0, or 10.0 mg/kg. Respiration was monitored by single-chamber plethysmography and apneas were scored as breaths longer than 2.5 seconds not preceded by a sigh. CAP increased apneas during non-rapid eye movement (NREM) sleep (p < 0.05 vs control) and reduced respiratory minute ventilation by about 15% in all behavioral states (waking, NREM, and REM sleep). We conclude that selective pharmacological activation of C-fibers produces a diathesis of sleep-disordered breathing specific to NREM sleep in rats.

Animals↗
PubMed1992

Effect of riboflavin-binding protein deficiency on riboflavin metabolism in the laying hen.

Normal chicken eggs contain substantial amounts of riboflavin, all of which is bound to a specific, high-affinity, riboflavin-binding protein (RfBP). Two hens, genetically unable to produce RfBP and thus unable to deposit sufficient riboflavin in their eggs, were compared to two normal hens with respect to the biological half-life of [14C]riboflavin, the tissue distribution of 14C-labeled flavins, and the relative contributions of tissue and dietary riboflavin to flavins deposited in the egg. The biological half-life of [14C]riboflavin was slightly but insignificantly less in the RfBP-deficient hens (11.5 +/- 1.7 days vs 15.1 +/- 3.3 days). The 14C-labeled flavin content of a variety of tissues 3 weeks after the intraperitoneal injection of 5 microCi of riboflavin was also very similar among the four hens. In contrast, the 14C-labeled flavin content of egg yolk, egg albumen, and blood plasma from RfBP-deficient birds was less than 10% of normal. For all hens, the specific radioactivity of flavins in yolk and albumen was similar to that in liver but less than that in heart. We conclude that riboflavin deposited in egg had equilibrated with the large hepatic flavin pool and was not derived preferentially from unlabeled dietary riboflavin. Other than the inability to deposit riboflavin in their eggs, hens of the mutant strain have normal riboflavin metabolism.

Administration, Oral↗