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PubMed2006

Peripheral immune activation by lipopolysaccharide decreases neurotrophins in the cortex and hippocampus in rats.

Lipopolysaccharide (LPS), a cell wall component of Gram-negative bacteria, induces neuronal death, decreases neurogenesis, and impairs synaptic plasticity and memory, but the mechanisms for these effects are not well understood. We hypothesize that neurotrophin levels in the brain are influenced by LPS. To test this hypothesis, we determined effects of LPS on brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and NT-3 levels in the brain after intraperitoneal injection of saline or LPS (0.1, 0.3 or 1.0mg/kg) in rats. LPS significantly decreased BDNF in the hippocampus (-20%), frontal cortex (-19%), parietal cortex (-63%), temporal cortex (-29%), and occipital cortex (-41%). LPS also significantly decreased NGF levels by 10-20% in the hippocampus and different cortical regions, except in the occipital cortex. Finally, LPS decreased NT-3 by 15-25% in the frontal cortex. These observations indicate that the neuroprotection mediated by neurotrophins in the brain are compromised by systemic immune activation induced by LPS.

Animals↗
PubMed2005

Pre- or post-training administration of the NMDA receptor blocker MK-801 impairs object recognition memory in rats.

The aim of the present study was to investigate the effects of NMDA receptor blockade on formation of object recognition memory. In the first experiment, adult Wistar rats were given an intraperitoneal injection of saline or the NMDA receptor antagonist [(+)-5-methyl-10,11-dihydro-5H-dibenzo-[a,d]cyclo-hepten-5,10-imine-maleate] (MK-801) (0.001, 0.01, or 0.1 mg/kg) 20 min prior to training in a novel object recognition task. In the second experiment, saline or MK-801 (0.1 mg/kg) were given immediately after training. Memory retention was tested 1.5 and 24 h after training. MK-801 impaired both short- and long-term retention of object recognition memory when given either before or after training. The results suggest that NMDA receptor activation is necessary for formation of object recognition memory.

Animals↗
PubMed2003

Acute effects of PYY3-36 on food intake and hypothalamic neuropeptide expression in the mouse.

It has recently been suggested that gut-derived PYY(3-36) may be involved in the central mediation of post-prandial satiety signals. We have examined the acute effects of peripherally administered PYY(3-36) on food intake and hypothalamic gene expression of neuropeptides in mice. A single intraperitoneal injection of PYY(3-36) to mice that had been fasted for 24h resulted in a highly significant reduction in food intake at 6 and 24h post-injection but not at 48h. However, in freely fed mice, food intake was unaltered by PYY(3-36) administration. In the arcuate nucleus POMC mRNA expression was significantly elevated at 6h and remained elevated at 24h following PYY(3-36) injection. By contrast NPY mRNA expression in the arcuate nucleus was suppressed at 6h but not at 24h post-injection. In the lateral hypothalamus there were no differences in MCH mRNA expression at either time point. In conclusion, peripherally administered PYY(3-36) has a suppressive effect on food intake that is more prominent in recently fasted mice and lasts up to 24 h. This is associated with a short-lived suppression of NPY mRNA, a longer lasting increase in POMC mRNA but no change in MCH mRNA expression.

Adaptation, Physiological↗
PubMed2004

Treatment with leucine stimulates the production of hepatocyte growth factor in vivo.

Hepatocyte growth factor (HGF) has pleiotropic effects. Up-regulation of HGF activity in vivo may be beneficial. Branched-chain amino acids (BCAAs) are known to modulate various cellular functions. When starved rats received intraperitoneal injections of valine, leucine or isoleucine, only leucine treatment increased both hepatic and circulating levels of HGF in a dose-dependent manner, up to 1.5 and 2.3 times higher, respectively, than in controls. When young growing rats with free access to food were injected with leucine once a day for a week, HGF levels and liver weights were significantly higher than those of control rats. Furthermore, 1 week of leucine treatment of adult rats resulted in elevated serum albumin levels with an increase in HGF levels. Taken together with our previous report showing that leucine stimulates HGF production by hepatic stellate cells in culture, leucine, among BCAAs, may induce an increase in HGF production by the liver in vivo.

Animals↗
PubMed2005

Inhibition of mTOR signaling with rapamycin attenuates renal hypertrophy in the early diabetic mice.

Early diabetic nephropathy is characterized by renal hypertrophy that is mainly due to proximal tubular hypertrophy. Mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase, and its signaling has been reported to regulate protein synthesis and cellular growth, specifically, hypertrophy. Therefore, we examined the effect of mTOR signaling on diabetic renal hypertrophy by using the specific inhibitor for mTOR, rapamycin. Ten days after streptozotocin-induced diabetes, mice showed kidney hypertrophy with increases in the phosphorylation of p70S6kinase and the expression of cyclin kinase inhibitors, p21(Cip1) and p27(Kip1), in the kidneys. The intraperitoneal injection of rapamycin (2 mg/kg/day) markedly attenuated the enhanced phosphorylation of p70S6kinase, the increment of cyclin-dependent kinase inhibitors, and renal enlargement without any changes of clinical parameters, including blood glucose, blood pressure, and food intake. Overexpression of a constitutive active form of p70S6kinase resulted in increased cell size of cultured mouse proximal tubule cells; thus, activation of p70S6kinase causes hypertrophy of proximal tubular cells. Our findings suggest that activation of mTOR signaling causes renal hypertrophy at the early stage of diabetes.

Animals↗
PubMed2005

Pharmacokinetic behaviour of ACP gel, an autocrosslinked hyaluronan derivative, after intraperitoneal administration.

Autocrosslinked polysaccharide (ACP) gel is a fully biocompatible cross-linked derivative of hyaluronic acid, which has prolonged in vivo residence time and improved mechanical properties with respect to native hyaluronan for use in various surgical applications. The objective of this study was to assess the pharmacokinetic behaviour of ACP gel in dogs after intraperitoneal administration. Seven beagle dogs received intraperitoneal injections of tritium-labelled ACP gel. Blood samples were taken, and urine and faeces were collected until sacrifice, scheduled at various time points from 3 to 192 h after administration. Organs were removed from the animals at autopsy. Bodily fluid and organ samples were analysed for total and non-volatile radioactivity. Non-volatile radioactivity slowly appeared in plasma, with a median T(max) of 12 h, and then declined with a mean half-life of 69 h. Total radioactivity in plasma peaked later and declined more slowly, consistent with the formation of tritiated water. Little non-volatile radioactivity was found in any organs except the liver, where about 16% of the dose was present 72 h after administration, and the intestines, where the presence of radioactivity was probably due to a retention effect. A minor amount of non-volatile radioactivity was also found in the bone marrow. In summary, ACP gel administered into the peritoneal cavity is removed slowly by active initial catabolism at the injection site, and is then catabolised by well described physiological pathway of hyaluronan degradation with final release of simple molecules such as CO(2) and H(2)O. Given its in vivo residence time, ACP gel may be considered an ideal implantable surgical device.

Absorbable Implants↗
PubMed2005

Preconditioning of the rat random-pattern skin flap: modulation by opioids.

Opioid receptors have been implicated in protecting several organ systems from ischaemic events. The authors have studied the effects of opioid receptors on random-pattern skin flap survival. Sixty-nine male Sprague-Dawley rats were used. Bipedicled dorsal skin flaps (2 x 8 cm) were elevated at the midline. Different doses of morphine (0.01, 0.1, 1 and 5 mg/flap) were administered locally in the cranial half of the flap and systemically through intraperitoneal injections (5 and 10 mg/kg). In another experiment, 0.4 mg/flap of naloxone was injected followed by 5 mg/flap injection of morphine to determine whether the effect of morphine is receptor mediated. The role of the opioid receptors in the ischaemic preconditioning (IPC) phenomenon was investigated by administration of naloxone (0.4 mg/flap) 1 h before clamping the cranial pedicle for 20 min followed by 40 min of reperfusion. Appropriate control groups were included. The cranial pedicle was cut 2 h after saline or drug administration in all groups and flap survival area was evaluated on the seventh postoperative day. Local administration of morphine in higher doses (1 and 5 mg/flap) significantly reduced the amount of flap necrosis when compared to that of the control cohort (P < 0.05). Naloxone abolished this protective effect of morphine. Furthermore naloxone significantly decreased the anti-ischaemic effect of the IPC. Systemic administrations of morphine had no significant effect on flap survival area in compare with the control group.

Animals↗
PubMed2003

Epileptogenic activity induced by histamine H(1) antagonists in amygdala-kindled rats.

The epileptogenic activities induced by histamine H(1) antagonists in amygdala-kindled rats were studied in comparison with activities in nonkindled rats (sham rats). Intraperitoneal injection of pyrilamine, diphenhydramine and ketotifen resulted in behavioral and electroencephalogram (EEG)-detected seizures in amygdala-kindled rats at doses which caused no or negligible seizures in sham rats. On the other hand, loratadine and cetirizine caused no behavioral or EEG seizures in either amygdala-kindled or sham rats even at a dose of 40 mg/kg. In conclusion, first-generation H(1) antagonists likely elicit epileptogenic activity in amygdala-kindled rats more potent than that in sham rats.

Amygdala↗
PubMed2004

Suppressive effects of milk-derived lactoferrin on psychological stress in adult rats.

Lactoferrin (LF) is known as an iron-binding glycoprotein. It has been shown that bovine LF (bLF) is transported into cerebrospinal fluid via blood although its physiological effects in the central nervous system (CNS) are still unclear. In this study, a suppressive effect of bLF on psychological distress was investigated in adult rats. Intraperitoneal injection of bLF (100 mg/kg) reduced stressful behaviors in a conditioned fear-induced freezing test and an elevated plus-maze test. Interestingly, the suppressive effect of bLF was enhanced by pretreatment with electric foot-shock (FS). This suppressive effect of bLF in the elevated plus-maze test was reversed by pretreatment with naloxone, an opioid receptor antagonist, at a dose of 1 mg/kg (ip). N(omega)-nitro-l-arginine methyl ester (l-NAME), a nitric oxide synthase (NOS) inhibitor, also blocked the suppressive effect of bLF and foot-shock. In addition, combined application of a low dose of bLF (30 mg/kg, ip) and l-arginine (30 and 100 mg/kg, ip) showed significant potentiated effects on psychological stress. These results suggest that bLF has suppressive effects on psychological distress, especially under the condition of moderate stress. Furthermore, it is suggested that bLF possibly activates an endogenous opioidergic system via nitric oxide synthase activation.

Analysis of Variance↗
PubMed2005

Peripheral lipopolysaccharide induces apoptosis in the murine olfactory bulb.

The olfactory bulb (OB) is one of the few structures in the adult mammalian CNS that contains a continuous supply of newly generated neurons in the subventricular zone. Therefore, the balance between the supply of new cells and apoptosis in the OB might determine olfactory function. Lipopolysaccharide-induced tumor necrosis factor (TNF)-alpha triggers the apoptotic cascade mediated by the TNF/TNF receptor (TNFR) pathway. The present study therefore examines the effect of the propagated innate immune reaction triggered by peripheral lipopolysaccharide on the OB of C3H/HeN mice. Within 2 h of an intraperitoneal injection of lipopolysaccharide, mRNA expression levels of the genes encoding IkappaB, TNF-alpha, and TNFR type 1 in the mouse OB were significantly enhanced. Double immunofluorescence microscopy confirmed that almost all TNF-alpha-immunopositive cells in the OB of the TNF-injected mice were located in the subependymal zone and that they overlapped cells immunostained with antibody against glial fibrillary acidic protein, but not with the antibody against F4/80, an antigenic marker of microglia. The number of TUNEL-positive cells identified exclusively in the granule cell layer was significantly increased in mice injected with lipopolysaccharide and sacrificed at 24 h thereafter. These results suggest that peripheral lipopolysaccharide causes disequilibrium between the supply and disappearance of the cells in the OB, which might lead to olfactory dysfunction.

Animals↗
PubMed2006

Central heme oxygenase-carbon monoxide pathway participates in the lipopolysaccharide-induced tolerance in rats.

Recently, heme oxygenase-carbon monoxide (HO-CO) pathway has been reported to be involved in the development of lipopolysaccharide (LPS) fever. However, no information exists about its participation in LPS tolerance, which is defined by an attenuation of the febrile response to repeated administrations of LPS. Thus, we tested the hypothesis that HO-CO pathway plays a role in endotoxin tolerance, which was induced by means of three consecutive LPS intraperitoneal injections (i.p.) at 24-h intervals. Body temperature (Tb) was measured by biotelemetry. Induction of the HO pathway using intracerebroventricular (i.c.v.) heme lysinate reversed tolerance, and this effect could be prevented by pretreatment with ODQ [a soluble guanylate cyclase (sGC) inhibitor; i.c.v.]. These results indicate that HO-CO pathway seems to be down-regulated during LPS tolerance, and that CO is the HO product that can prevent LPS tolerance, acting via cGMP. In further support, either biliverdine or iron (the others HO products; i.c.v.) had no effect in LPS-induced tolerance.

Animals↗
PubMed2005

Systemic administration of lipopolysaccharide and interleukin-1beta have different effects on memory consolidation.

Sickness behaviour is an adaptive response to infection that includes lethargy, anorexia and of direct relevance to this work, learning and memory impairments. It has been suggested that proinflammatory cytokines may disrupt learning and memory by interfering with memory consolidation [C.R. Pugh, K. Kumagawa, M. Fleshner, L.R. Watkins, S.F. Maier, J.R. Rudy, Selective effects of peripheral lipopolysaccharide administration on contextual and auditory-cue fear conditioning, Brain Behav. Immun. 12 (1998) 212-229]. We tested whether systemic interleukin-1beta is sufficient to induce impairments in memory consolidation by comparing the effects of post-learning administration of interleukin-1beta with, the potent endotoxin, lipopolysaccharide; and saline, on retention of conditioned fear of a context. We administered an acute intraperitoneal injection of lipopolysaccharide, interleukin-1beta or saline immediately following a single conditioning episode in which rats received two tone-shock pairings. Two days following the learning episode, animals were tested for strength of conditioned responding to both the context and tone. Lipopolysaccharide-injected animals, but not interleukin-1beta-injected animals, exhibited less conditioned fear of context compared to saline-treated controls. All groups showed similar conditioned fear of tone. Our results suggest that systemic interleukin-1beta is not sufficient to disrupt memory consolidation, but rather, the synergistic actions of the proinflammatory cytokines released by lipopolysaccharide are required to disrupt memory consolidation.

Acoustic Stimulation↗
PubMed2005

In vivo modification of adriamycin-induced apoptosis in L-5178Y lymphoma cell-bearing mice by (+)-alpha-tocopherol and superoxide dismutase.

Apoptosis was followed in L5178Y lymphoma cell-bearing mice at different times after intraperitoneal injections of adriamycin (ADM). Apoptosis was determined morphologically and confirmed by DNA laddering on electrophoresis. Apoptosis was observed 36h after injection of 5mg/kg ADM (apoptotic cell index 64.2+/-5.6 vs. 1.5+/-2.1 from the untreated group) and confirmed by DNA electrophoresis. However, when the animals were pretreated with (+)-alpha-tocopherol acid succinate or superoxide dismutase before ADM administration apoptotic index significantly diminished (P<0.05) and the DNA electrophoresis did not show fragmentations. We conclude that in ADM-treated mice, tumour cell death occurs in two ways: first by necrosis, then later by apoptosis. These observations are likely to be associated with or caused by the generation of reactive oxygen species.

Animals↗
PubMed2005

The endogenous peptide apelin potently improves cardiac contractility and reduces cardiac loading in vivo.

OBJECTIVE: The endogenous peptide apelin is differentially regulated in cardiovascular disease but the nature of its role in cardiac function remains unclear. METHODS: We investigated the functional relevance of this peptide using ECG and respiration gated magnetic resonance imaging, conductance catheter pressure-volume hemodynamic measurements, and echocardiography in vivo. In addition, we carried out histology and immunohistochemistry to assess cardiac hypertrophy and to localize apelin and APJ in the adult and embryonic mouse heart. RESULTS: Intraperitoneal injection of apelin (300 microg/kg) resulted in a decrease in left ventricular end diastolic area (pre: 0.122+/-0.007; post: 0.104+/-0.005 cm(2), p=0.006) and an increase in heart rate (pre: 537+/-20; post: 559+/-19 beats per minute, p=0.03). Hemodynamic measurements revealed a marked increase in ventricular elastance (pre: 3.7+/-0.9; post: 6.5+/-1.4 mm Hg/RVU, p=0.018) and preload recruitable stroke work (pre: 27.4+/-8.0; post: 51.8+/-3.1, p=0.059) with little change in diastolic parameters following acute infusion of apelin. Chronic infusion (2 mg/kg/day) resulted in significant increases in the velocity of circumferential shortening (baseline: 5.36+/-0.401; 14 days: 6.85+/-0.358 circ/s, p=0.049) and cardiac output (baseline: 0.142+/-0.019; 14 days: 0.25+/-0.019 l/min, p=0.001) as determined by 15 MHz echocardiography. Post-mortem corrected heart weights were not different between apelin and saline groups (p=0.5) and histology revealed no evidence of cellular hypertrophy in the apelin group (nuclei per unit area, p=0.9). Immunohistochemistry studies revealed APJ staining of myocardial cells in all regions of the adult mouse heart. Antibody staining, as well as quantitative real time polymerase chain reaction identified expression of both APJ and apelin in embryonic myocardium as early as embryonic day 13.5. CONCLUSIONS: Apelin reduces left ventricular preload and afterload and increases contractile reserve without evidence of hypertrophy. These results associate apelin with a positive hemodynamic profile and suggest it as an attractive target for pharmacotherapy in the setting of heart failure.

Animals↗
PubMed2004

The antioxidant and antifibrogenic effects of the glycosaminoglycans hyaluronic acid and chondroitin-4-sulphate in a subchronic rat model of carbon tetrachloride-induced liver fibrogenesis.

Hepatic fibrosis involves the interplay of many factors including reactive oxygen species. Recent reports described antioxidant properties of glycosaminoglycans (GAGs). Since several findings have shown that hyaluronic acid (HYA) and chondroitin-4-sulphate (C4S) may act as antioxidant molecules, the aim of this research was to evaluate the antioxidant effects of HYA and C4S treatment in a rat model of liver fibrosis. The effect on tissue inhibitors of metalloproteinases (TIMPs) was also studied. Liver fibrosis was induced in rats by eight intraperitoneal injections of CCl4, twice a week for 6 weeks. HYA or C4S alone (25 mg/kg) or HYA and C4S in combination (12.5 + 12.5 mg/kg) were administered daily by the same route during the 6 weeks. At the end of the 6-week treatment period (24 h after the last dose of GAGs), the following parameters were evaluated: (1) serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, as index of hepatic cell disruption; (2) hepatic conjugated dienes (CD), as index of lipid peroxidation; (3) hepatic TIMPs activity and expression; (4) hepatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity, as index of endogenous defences; (5) hepatic hydroxyproline, as index of collagen deposition. CCl4-induced liver fibrosis enhanced lipid peroxidation and TIMPs activation, increased ALT and AST, depleted antioxidants SOD and GPx, and caused collagen deposition in liver tissue. Treatment with GAGs, especially when in combination, successfully reduced ALT and AST rise, lipid peroxidation by evaluating conjugated dienes, TIMPs activation and mRNA expression, partially restored SOD and GPx activities, and limited collagen deposition in the hepatic tissue. The data obtained showed that these molecules were able to limit hepatic injury induced by chronic CCl4 intoxication and especially limited liver fibrosis. They also confirm that HYA and C4S may exert antioxidant mechanism, while reduction of TIMPs expression suggests that GAGs may influence MMPs and TIMPs imbalance in liver fibrosis.

Alanine Transaminase↗
PubMed2004

Prior PCB exposure suppresses hypoxia-induced up-regulation of glycolytic enzymes in Fundulus heteroclitus.

Increased activity of the glycolytic enzymes is a conserved feature of the cellular response to hypoxia, and may represent a protective mechanism by which cells can survive short-term hypoxic exposure. Gene induction by hypoxia involves a dimer of the hypoxia inducible factor (HIF)-1 alpha and the nuclear cofactor HIF-1 beta, also called the aryl hydrocarbon receptor nuclear translocator (ARNT), which is also involved in induction of genes in response to aryl hydrocarbon exposure. To assess the possibility of interaction between these pathways, we examined changes in the activity of the glycolytic enzymes in response to hypoxia and polychlorinated biphenyl (PCB) exposure in the liver of a teleost fish, Fundulus heteroclitus. After 3 days of hypoxic exposure (dissolved oxygen levels between 1.5 and 2.0 mg/L), there were significant increases in the activity of six glycolytic enzymes (PGI, ALD, TPI, PGK, PGM and LDH). In contrast, intraperitoneal injection of 1 microg/g body weight of PCB #77 (3,3',4,4'-tetrachlorobiphenyl) caused significant decreases in glycolytic enzyme activity after 7 days of exposure. When fish were injected with PCB #77 and then (4 days later) exposed to hypoxia for 3 days as before, we observed no induction of the glycolytic enzymes. This suggests that there is an antagonistic interaction between exposure to PCBs and hypoxia in F. heteroclitus. Prior PCB exposure could make these fish less tolerant of environmental hypoxia.

Animals↗
PubMed2005

A non-lethal method to estimate CYP1A expression in laboratory and wild Atlantic salmon (Salmo salar).

Expression of cytochrome P4501A (CYP1A) has been used as a biomarker for possible exposure to contaminants such as PCBs and dioxins in teleost fish. Using a quantitative reverse transcription-polymerase chain reaction (Q-RT-PCR) and a non-lethal gill biopsy, we estimated levels of CYP1A mRNA expression in Atlantic salmon (Salmo salar). Groups of ten Atlantic salmon juveniles (48-76 g) received an intraperitoneal injection of 50 microg g(-1) beta-naphthoflavone (BNF) or vehicle. Their gill tissues were repeatedly sampled by non-lethal biopsies on day 0, 1, 2 and 7. Control fish expressed basal levels of CYP1A over the duration of sampling. BNF-treated salmon demonstrated similar levels of CYP1A to control fish at day 0 and higher levels over the course of each additional sampling point. Gill biopsies from wild salmon sampled from Millers River (South Royalston, Worcester County, MA, USA), known to contain PCBs, showed significantly higher CYP1A levels over an uncontaminated reference stream, Fourmile Brook (Northfield, Franklin County, MA, USA). We conclude that gill biopsies coupled with Q-RT-PCR analysis is a valuable tool in environmental assessment of wild Atlantic salmon populations and has the potential to be applied to other populations of fish as well.

Animals↗
PubMed2003

The potential beneficial effect of leptin on an experimental model of hyperlipidemia, induced by chronic ethanol treatment.

BACKGROUND: Obesity is known to predispose individuals to liver disease by increasing hepatic sensitivity to endotoxin. The aim of the present study was to determine the effect of mouse recombinant leptin on food intake, body weight, hepatic and plasma lipids and lipoproteins in alcohol-induced liver injury. METHOD: Male Swiss mice weighing 28-32 g were administered ethanol (6.32 g x kg(-1) body weight, p.o.) for the first 30 days. Subsequently, ethanol-fed mice were given intraperitoneal injections of exogenous leptin (230 microg x kg(-1) body weight, i.p.) every alternate day for 15 days. At the end of the total experimental period of 45 days, plasma concentrations of total cholesterol, free fatty acids, triglycerides, lipoprotein lipase and lipoproteins were measured. RESULTS: Exogenous leptin injections to alcohol-fed mice significantly (P<0.05) inhibited the rise in hepatic and plasma lipid and lipoprotein concentrations as compared with those of the unsupplemented ethanol fed mice. Food intake and average body weight at the end of the experimental period was significantly decreased on leptin administration. CONCLUSION: Chronic administration of exogenous mouse recombinant leptin prevents the rise in lipids and lipoprotein concentrations significantly in an animal model of alcohol-induced hyperlipidemia.

Administration, Oral↗