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PubMed2002

Paclitaxel-loaded crosslinked hyaluronic acid films for the prevention of postsurgical adhesions.

PURPOSE: Post surgical adhesion formation results in significant morbidity for surgical patients. The purpose of this study was to investigate the use of paclitaxel (PTX) as an inhibitor of adhesion formation in rats and to design and characterize a controlled release film formulation of the drug for application to exposed surgical sites. METHODS: The rat cecal side wall abrasion model was used to investigate the anti-adhesion properties of PTX. The drug was administered by either intraperitoneal injection (i.p.), as the cremophor formulation (Taxol) or by application of carbodiimide crosslinked hyaluronic acid (HA) films containing PTX. The HA films were also characterized by measurements of elasticity, degree of swelling in water and drug release rates. RESULTS: Taxol administered by i.p. injection at 4 mg/kg on a daily basis for between 3 and 5 days resulted in a significant reduction in adhesion formation. All animals in the control group (n = 10) had some form of adhesion following abrasion whereas the percent of animals without adhesions significantly increased and the mean incidence of adhesion formation decreased in the three Taxol treated groups. The application of 5% PTX loaded HA films had a similar significant effect in increasing both the % of animals without adhesions and in reducing the mean incidence of adhesions. CONCLUSIONS: Paclitaxel is an effective inhibitor of adhesion formation in rats. HA crosslinked with 2 mM water soluble carbodiimide and containing 10% glycerol and 5% PTX are flexible, mucoadhesive, biocompatible controlled release films suitable for application to surgical sites for the prevention of adhesion formation.

Animals↗
PubMed1989

Protein precoating of polylactide microspheres containing a lipophilic immunopotentiator for enhancement of macrophage phagocytosis and activation.

Biodegradable microspheres containing a lipophilic muramyl dipeptide, MDP-B30, were prepared from a L-lactic acid-glycolic acid copolymer. The effect of precoating the microspheres with water-soluble polymers including proteins on the antitumor activity of mouse peritoneal macrophages (M phi) was investigated. Macrophages activated by phagocytosis of the microspheres exhibited growth inhibitory activity toward Meth-A tumor cells. The activity correlated with the extent of M phi phagocytosis of the microspheres. M phi phagocytosis was greatly augmented by gelatin precoating of the microspheres, resulting in a significant increase of in vitro antitumor activity of M phi by the microspheres. However, potentiation of M phi activity by gelatin precoating was minimal after intraperitoneal injection of the microspheres, but cross-linking of the coated gelatin with glutaraldehyde afforded potentiation of the antitumor activity in vivo.

Adjuvants, Immunologic↗
PubMed2002

Effect of hyperosmolar mannitol on convection-enhanced delivery into the rat brain stem.

INTRODUCTION: Convection-enhanced delivery (CED) can safely achieve high local infusate concentrations within the rat brain stem with predictable distribution volumes. The authors investigated the effects of co-infusion or systemic administration of hyperosmolar mannitol on distribution parameters for infusions into the rat brain stem. METHODS: Fifteen rats underwent stereotactic cannula placement into the pontine nucleus oralis (PnO) followed by infusions at a constant rate to a total volume of 1 microl. Five rats underwent infusion of fluorescein isothiocyanate (FITC)-dextran diluted in 20% mannitol. Five rats received an intraperitoneal injection of 20% mannitol 10 min prior to infusion of FITC-dextran diluted in isotonic saline. As a control group, 5 rats underwent infusion of FITC-dextran diluted in isotonic saline without mannitol administration. Serial brain sections were imaged using confocal microscopy with ultraviolet illumination, and distribution volume (Vd) was calculated by computer image analysis. Histologic analysis was performed on adjacent sections. RESULTS: Volumes of distribution were not significantly increased by co-infusion of mannitol directly into the brain stem or by systemic mannitol administration compared to infusion without mannitol. Similarly, mannitol administration by either means failed to significantly alter maximal cross-sectional area or cranio-caudal extent of fluorescence. No animal demonstrated a postoperative neurological deficit or histologic evidence of tissue disruption. CONCLUSIONS: Neither systemic administration nor co-infusion of hyperosmolar mannitol significantly affects distribution parameters for CED infusions into the rat brain stem.

Animals↗
PubMed1998

Delayed gastric emptying by Helicobacter pylori lipopolysaccharide in conscious rats.

The present study was carried out to investigate the possibility that lipopolysaccharide deprived from Helicobacter pylori may alter gastric motility. To address the question, we examined the effect of H. pylori lipopolysaccharide on gastric emptying in conscious rats. Gastric emptying was evaluated by the phenol red method. Time-course and dose-related effects of intraperitoneal administration of H. pylori lipopolysaccharide were investigated. Intraperitoneal injection of H. pylori lipopolysaccharide significantly suppressed gastric emptying of a liquid meal in a dose-dependent manner. The inhibitory action of H. pylori lipopolysaccharide was observed 2, 4, 8, or 12 hr after the injection. These results suggest for the first time that H. pylori lipopolysaccharide may suppress gastric emptying in a long-lasting fashion. It is also suggested that H. pylori may influence gastric function through its cell wall structure named lipopolysaccharide.

Animals↗
PubMed1994

Activation of Fc receptor-mediated phagocytosis by mouse peritoneal macrophages following the intraperitoneal administration of liposomes.

The effects of liposomes on the phagocytic activity of mouse peritoneal macrophages were investigated using IgG-opsonized sheep red blood cells (SRBC). The highest ingestion index of opsonized SRBC via Fc receptors of macrophages from BALB/c mice was observed for macrophages harvested on day 4 following the intraperitoneal injection of liposomes (2.27 mumol lipid/mouse). An increase in the ingestion index was observed irrespective of liposomal charge. Binding parameters of Fc receptors of macrophages from liposome- or saline-injected mice were determined using horseradish peroxidase-conjugated IgG, and an increase in the number of binding sites with the same binding constant was observed in macrophages from liposome-injected mice. The activation mechanism of mouse peritoneal macrophages by liposomes differed from that by lipopolysaccharides. Liposomes thus appear to contribute to the activation of immune response.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2003

Cytotoxicity of streptozotocin on neuroendocrine cells of the pancreas and the gut.

Streptozotocin has been used to induce diabetes mellitus in experimental animals and has been thought to have a selective cytotoxic effect on the beta-cells in the islets of Langerhans. The aim of the present study was to determine whether streptozotocin has any cytotoxic effect on other neuroendocrine cells of the gastrointestinal tract. Eight female Sprague-Dawley rats received intraperitoneal injections of 100 mg/kg streptozotocin in citric acid buffer; the concentration of streptozotocin was adjusted to 25 mg/ml buffer. Seven rats, serving as controls, received an equivalent volume of the vehicle. The rats were killed after three days and the fundus, antrum, small intestine and pancreas were examined for neuroendocrine cells. Our study confirms that streptozotocin is cytotoxic towards beta-cells. In addition, it is cytotoxic towards neuroendocrine cells of the oxyntic mucosa of the stomach. This finding may have clinical significance and suggests that streptozotocin may be used in the treatment of gastric neuroendocrine tumors as well as insulinomas.

Animals↗
PubMed2003

Alterations in NMDA receptor subunit levels in the brain regions of rats chronically administered typical or atypical antipsychotic drugs.

It has been hypothesized that glutamatergic neurotransmission is related to the therapeutic effect of antipsychotic drugs. To test this hypothesis, we measured by use of the Western blot technique the polypeptide levels of NMDA receptor subunits, that is, NMDAR1, 2A, 2B, and 2C, in several regions of the rat brain after chronic treatment with haloperidol (HPD) or clozapine (CLZ). Each rat was intraperitoneally injected with HPD or CLZ at 10:00 h daily for 14 days. The brain regions examined were frontal cortex, striatum, nucleus accumbens, hippocampus, and cerebellum. Decreases in the polypeptide level of NMDAR2B were seen in hippocampus (but not in other brain regions) following the treatment with HPD or CLZ. Altered levels in NMDAR1-, 2A-, and 2C were not detected in any brain regions examined. We infer that an alteration in NMDAR2B in hippocampus is related to therapeutic effects of antipsychotic drugs.

Animals↗
PubMed1999

Effect of 5-fluorouracil on gastrointestinal carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats.

This study was undertaken to determine the effect of 5-fluorouracil on gastrointestinal carcinogenesis. Sixty rats were divided into three groups of 20 rats each. All rats were exposed to N-methyl-N'-nitro-N-nitrosoguanidine for the first 20 weeks. Group 1 rats received intraperitoneal injections of 5-fluorouracil for the first 20 weeks and were then observed for the second 20 weeks. Group 2 rats also received 5-fluorouracil injections, but for the second 20 weeks. Group 3 rats received no 5-fluorouracil treatment. Four of 20 rats in group 1 developed an invasive adenocarcinoma. In group 3, invasive squamous cell carcinoma and adenocarcinoma developed in one rat each. None of the group 2 rats had malignant lesions. These results suggested that 5-fluorouracil is not effective in suppressing the initial stage of gastrointestinal carcinogenesis with a coexisting carcinogen. Rather, the therapeutic effect is exerted in later stages of tumor progression.

Adenocarcinoma↗
PubMed1997

Cytokine and nitric oxide production in the acute phase of bacterial cell wall-induced arthritis.

We have investigated the temporal relationship among proinflammatory cytokine expression, nitric oxide (NO) production and joint inflammation in the acute phase of bacterial cell wall-derived peptidoglycan polysaccharide (PG/PS)-induced arthritis. Acute joint inflammation was induced in female LEW/N rats by a single intraperitoneal injection of PG/PS. Arthritis index and paw volume were quantified and joint histopathology was evaluated during acute joint inflammation (0-10 days). Tumor necrosis factor (TNF), interleukin-1 (IL-1) and interleukin-6 (IL-6) were determined by bioassay whereas nitric oxide (NO) was quantified by measuring serum nitrate/nitrite levels via the Griess procedure. We found that serum levels of TNF and serum IL-1 preceded the increase in IL-6 and NO production. Furthermore, the production of these proinflammatory cytokines and NO preceded bone erosion and osteoclast activity. Erosion of subchondral bone preceded pannus formation and cellular synovitis in the acute phase of PG/PS-induced arthritis. The temporal expression of TNF, IL-1, IL-6 and NO suggest a cascade of inflammatory mediators in which monocytes and macrophages respond to PG/PS with enhanced synthesis of TNF and IL-1, which may in turn promote the synthesis of IL-6 and NO. We postulate that one or more of these inflammatory events are responsible for initiating the subchondral bone erosion observed in acute joint inflammation.

Acute Disease↗
PubMed2003

Secretory activity of mast cell during stress: effect of prolyl-glycyl-proline and Semax.

Stress increased secretory activity of mast cells in the mesentery and subcutaneous fat of rats. Intraperitoneal injection of Semax and prolyl-glycyl-proline in doses of 0.05 and 1 mg/kg, respectively, 1 h before stress abolished this effect. The test preparations did not modulate secretory activity of mast cells in unstressed animals. Semax and prolyl-glycyl-proline in vitro prevented activation of mast cells with synacten and acetylcholine. The stabilizing effect of peptides on mast cells probably determines their antiulcer activity.

Acetylcholine↗
PubMed2004

Interstitial infusion of carmustine in the rat brain stem with systemic administration of O6-benzylguanine.

Interstitial infusion of carmustine (BCNU) into the rat brain stem in conjunction with systemic administration of O6-benzylguanine (O6-BG) was performed in an effort to assess clinical tolerance. A total of 12 rats underwent stereotactic cannula placement into the pontine segment of the brain stem. Six of the rats underwent a 24-h infusion of BCNU (Volume of infusion [Vi] 200 microl) at its maximal concentrated dose (3.3 mg/ml) in 5% dextrose water. Six additional rats underwent 24-h infusion of BCNU preceded by an intraperitoneal injection of O6-BG at a dose of 50 mg/kg. Serial neurological examinations were performed on all animals. Histologic analyses were performed immediately or 2 weeks following sacrifice. Postoperatively, there were no neurological changes in any of the animals. Postmortem histological examination of the brains showed small pontine cavitary lesions (ranging from 20 to 250 microm) containing variable numbers of macrophages or neutrophils consistent with an inflammatory response. No changes beyond these findings indicated any histological evidence of injury. These finding were limited only to the cannula site and no changes beyond region of the cannula tract were found. These findings indicate that interstitial infusion of BCNU into the brain stem in conjunction with systemic administration of O6-BG is safe in a small animal and may serve as a potential investigative strategy for children with diffuse pontine gliomas.

Animals↗
PubMed2004

T-588 protects motor neuron death following axotomy.

R(-)-1-(benzo [b] thiophen-5-yl)-2-[2-(N,N-diethylamino)ethoxy] ethanol hydrochloride) (T-588) enhances acetylcholine release. This compound slows the motor deterioration of wobbler mouse motor neuron disease and enhances neurite outgrowth and choline acetyltransferase activity in cultured rat spinal motor neurons. We examined the ability of T-588 on axotomized spinal motor neuron death in the rat spinal cord. After the postnatal unilateral section of sciatic nerve, there was approximately a 50% survival of motor neurons in the fourth lumbar segment. In comparison with vehicle, intraperitoneal injection of T-588 for 14 consecutive days rescued spinal motor neuron death. Our results showing in vivo neurotrophic activity of T-588 for motor neurons support the applicability of T-588 for the treatment of motor neuron diseases, such as amyotrophic lateral sclerosis and motor neuropathies.

Animals↗
PubMed2003

Effects of spermine-conjugated Bowman-Birk inhibitor (spermine-BBI) on carcinogenesis and cholesterol biosynthesis in mice.

PURPOSE: The goals of the studies reported here were to evaluate the effects of the soybean-derived protease inhibitor known as the Bowman-Birk inhibitor (BBI) and its spermine-conjugate (spermine-BBI) on the prevention of lung tumorigenesis and the reduction of heart disease parameters. METHODS: Both spermine-BBI and purified BBI (pBBI), at a dose of 20 mg/kg body weight, were administered as intraperitoneal injections to animals treated with the chemical carcinogen 3-methylcholanthrene (MCA) to determine their effects on chemically induced lung tumorigenesis in A/J mice. In addition, the effects of spermine-BBI and pBBI on the aortic cholesterol content and the percent ester in the mice were determined. RESULTS: The characteristics of the animals in the various treatment groups were comparable in terms of behavioral phenomena, weight gain, and lack of deaths during the experimental period. Thus, there was no detectable toxicity in spermine-BBI-treated mice. Both spermine-BBI and pBBI had a significant suppressive effect on MCA-induced lung tumors, with spermine-BBI being more effective than pBBI. Spermine-BBI was considerably more effective than pBBI at affecting heart-disease-related parameters. The amount of esterified cholesterol present in the aortas of mice treated with spermine-BBI was 9% lower than that of the controls. Both pBBI and spermine-BBI reduced total cholesterol levels in the blood, with pBBI reducing the cholesterol level by 15.5% and spermine-BBI by 33.3%. CONCLUSIONS: Spermine-BBI can prevent lung carcinogenesis without detectable toxic effects; therefore, it is concluded that lung targeting by the cationization of polypeptides can be achieved without apparent toxicity. The increase in retention of spermine-BBI compared to pBBI in liver tissue may make a difference for the heart disease parameters evaluated. Although spermine-BBI is capable of reducing the total cholesterol and ester levels in mice, pBBI did not have as great an effect on these parameters. Because the liver is the major site for the production of cholesterol, the localization of spermine-BBI in liver tissue may account for the greater effect of spermine-BBI on blood cholesterol levels. Spermine-BBI was administered to animals for only the first 2 months of the 4-month assay period before animal sacrifice, so the results suggest that the effects of spermine-BBI on the parameters related to heart disease are long-lasting, as are the effects of both pBBI and spermine-BBI on lung tumorigenesis.

Animals↗
PubMed2002

The matrix metalloproteinase inhibitor batimastat inhibits the lung colonisation of orthotopically implanted malignant pancreatic tumor cells in SCID mice.

AIM OF STUDY: In this study, we investigated the effect of the matrix metalloproteinase inhibitor batimastat on the lung colonisation of orthotopically implanted malignant pancreatic tumor cells in SCID mice. MATERIAL AND METHODS: Following intraperitoneal anaesthesia, 10(6) Panc-TU-1 cells were orthotopically implanted in the head of the pancreas in 20 SCID mice. Seven days later, treatment of 10 of these mice with an intraperitoneal injection of batimastat (30 mg/kg body weight) was begun and continued for 14 days. Of the mice in the untreated control group, 3 were sacrificed and examined after 7 days, a further 3 after 14 days and the remainder together with the group that had been treated after 21 days. RESULTS: Tumor growth was clearly visible between the 14th. and the 21st. postoperative day. The orthotopically implanted tumor cells metastasized between the 2nd. and 3rd. postoperative week in the lung. In the control group, a diffuse metastasis of the lung was observed, but in the group of treated mice no lung metastases were found. CONCLUSION: In this mouse model, a clear reduction and inhibition of lung metastases from orthotopically implanted pancreatic tumor cells was achieved by treatment with the matrix metalloproteinase inhibitor batimastat.

Animals↗
PubMed2001

Histometric evaluation of the effect of nicotine administration on periodontal breakdown: an in vivo study.

The present study investigated the effect of nicotine administration on periodontal breakdown resulting from ligature-induced periodontitis in rats. Twenty adult male Wistar rats were used. After anesthesia, a mandibular first molar was randomly assigned to receive a cotton ligature in the sulcular area while the contralateral tooth was left unligated. The animals were randomly assigned to one of the following treatments. of daily intraperitoneal injections: A - saline solution, B -0.37 mg of nicotine kg, C -0.57 mg of nicotine kg and D -0.73 mg of nicotine/kg. Thirty days later, the animals were sacrificed and the specimens routinely processed for serial decalcified sections. Statistical analysis (ANOVA) revealed greater bone loss (p<0.05) in the ligated teeth of animals which received nicotine (groups B/C D) than in the ligated teeth of animals which received saline solution (group A). In addition, a dose-dependent response was observed among the nicotine groups. A negative effect of nicotine was observed in the unligated teeth of the experimental groups (p<0.05). Therefore, daily administration of nicotine enhanced, in a dose-dependent manner, the effects of local factors in producing periodontal breakdown. Furthermore, the nicotine seemed to have a direct deleterious effect on the periodontal tissues.

Alveolar Bone Loss↗
PubMed2003

Stress may enhance nicotine effects on periodontal tissues. An in vivo study in rats.

OBJECTIVES AND BACKGROUND: Diabetes mellitus and smoking have been described as important risk factors that may affect the initiation and progression of periodontitis. Recent studies have pointed to potentially periodontal risk indicators, which include stress. The present study investigated the effects of stress associated with nicotine administration on periodontal breakdown resulting from ligature-induced periodontitis in rats. METHODS: Twenty adult male Wistar rats were used. After anesthesia, both mandibular first molars received a cotton ligature in the dento-gingival area. The animals were randomly assigned to one of the following experimental groups: A - saline solution, B - 0.73 mg of nicotine/kg/d (intraperitoneal), C - stress (immobilization - 2 h/d/40 d) associated with an intraperitoneal administration of saline solution, and D - stress (immobilization - 2 h/d/40 d) associated with an intraperitoneal injection of 0.73 mg of nicotine/kg/d. Forty days later, the animals were sacrificed and the specimens routinely processed for serial decalcified sections. RESULTS: Intergroup analysis (ANOVA) revealed a greater bone loss (P < 0.05) in the animals of group D compared with the animals from groups A, B and C. In addition, the data revealed a significant effect of nicotine (group B) compared with groups A and C (P < 0.05), and no difference between groups A and C (P > 0.05). CONCLUSION: Within the limits of the present study, although stress did not affect periodontitis by itself, it significantly enhanced the effects of nicotine on the periodontal tissues.

Alveolar Bone Loss↗
PubMed2000

Aloe-Emodin quinone pretreatment reduces acute liver injury induced by carbon tetrachloride.

Aloe contains several active compounds including aloin, a C-glycoside that can be hydrolyzed in the gut to form aloe-emodin anthrone which, in turn, is auto-oxidized to the quinone aloe-emodin. On the basis of the claimed hepatoprotective activity of some antraquinones, we studied aloe-emodin in a rat model of carbon tetrachloride (CCl4) intoxication, since this xenobiotic induces acute liver damage by lipid peroxidation subsequent to free radical production. Twelve rats were treated with CCl4 (3 mg/kg) intraperitoneally and six were protected with two intraperitoneally injections of aloe-emodin (50 mg/kg; CCl4+aloe-emodin); six other rats were only aloe-emodin injected (aloe-emodin) and six were untreated (control). Histological examination of the livers showed less marked lesions in the CCl4+aloe-emodin rats than in those treated with CCl4 alone, and this was confirmed by the serum levels of L-aspartate-2-oxoglutate-aminotransferase (394+/-38.6 UI/l in CCl4, 280+/-24.47 UI/l in CCl4+aloe-emodin rats; P<0.05). We also quantified changes in hepatic albumin and tumour necrosis factor-alpha mRNAs. Albumin mRNA expression was significantly lower only in the liver of CCl4 rats (P<0.05 versus control) and was only slightly reduced in the CCl4+aloe-emodin rats. In contrast tumour necrosis factor-alpha mRNA was significantly higher (P<0.05) in the CCl4 than the control rats and almost equal in the CCl4+aloe-emodin, aloe-emodin and control groups. In conclusion, aloe-emodin appears to have some protective effect not only against hepatocyte death but also on the inflammatory response subsequent to lipid peroxidation.

Albumins↗