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The role of nucleolar stress in the anti-tumour activity of non-steroidal anti-inflammatory drugs (NSAIDs)Lobb, Ian Thomas January 2014 (has links)
Overwhelming evidence indicates that aspirin (ASA) and related non-steroidal anti-inflammatory drugs (NSAIDs) have anti-tumour activity against colorectal cancer (CRC). Although the underlying mechanisms have yet to be fully elucidated, the host laboratory have shown that nucleolar sequestration of the NF-κB component RelA is critical. In the course of these studies, it was noted that alongside effects on the NF- κB pathway, ASA has a profound effect on nucleoli, including a dramatic increase in nucleolar size. These data were particularly interesting as, in addition to its role in ribosome biogenesis, the nucleolus is known to act as a stress sensor and play a key role in the regulation of cell growth and apoptosis. Indeed, this organelle has been identified as a potential target for anti-tumour agents. However, how stress causes changes to nucleolar function, and how these are translated into changes in cell phenotype, remain unclear. Therefore, the aim of my thesis was to fully characterise ASA effects on nucleoli and to determine whether these effects contribute to the anti-tumour activity of this agent. I found that ASA induced an atypical form of nucleolar stress that was associated with enlargement of the organelle, relocalisation of nucleolar markers to the periphery, depletion of the critical component of the Pol I transcription factor complex, TIF-IA, and inhibition of rRNA transcription. These effects were independent of the p38 and JNK2 MAP kinase pathways. However, they were mimicked by inhibition of CDK4, which had previously been shown to lie upstream of ASA effects on the NF-κB pathway. These data describe a novel mechanism by which ASA, and CDK4 inhibition, may inhibit the growth of colon cancer cells. In addition to this candidate approach, I used Stable Isotope Labelling by Amino acids in Cell culture (SILAC) based quantitative proteomics to obtain a global overview of ASA effects on nucleoli of colon cancer cells. Firstly, a protocol was successfully developed to isolate pure nucleoli from SW480 CRC cell lines. This protocol was then applied to SILAC labelled cells treated with ASA for three time-points (0, 6, 10 h). In collaboration with R.T Hay and M. Tatham (University of Dundee), proteomic analysis was then carried out by tandem-mass spectrometry. These data confirmed that ASA has a significant effect on the nucleolar proteome. They also revealed that ASA induces a distinct type of nucleolar stress that is associated with the accumulation of chaperones, translational regulators and members of the ubiquitin-proteasome system (UPS) in this organelle. These data were reminiscent of studies previously published on the effect of proteasome inhibition on nucleoli. I therefore used SILAC-based proteomics to compare ASA effects on nucleoli to those induced by the proteasome inhibitor, MG132. I found that similar sub-groups of proteins accumulate in nucleoli in response to both agents and that ASA induced proteotoxic stress in a similar manner to MG132. Fluorescence correlation spectroscopy in collaboration with R. Duncan and K. Martin (Heriot-Watt University) demonstrated the relative reduction in mobility of nucleolar DsRed-RelA, indicating that, similar to MG132, ASA induces formation of nucleolar aggresomes. Mechanistic studies suggested that blocking ASA-mediated proteotoxic stress blocked the apoptotic effects of the agent. Taken together, these data define a distinct type of nucleolar stress that may be involved in the cells response to proteotoxic stress and be required for the anti-tumour activity of ASA.
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NITROGEN OXIDE RELEASING PRODRUGS AS ANTIINFLAMMATORY, ANTICANCER AND CARDIOPROTECTIVE AGENTSBasudhar, Debashree January 2011 (has links)
This dissertation focuses on chemical and biological evaluation of diazeniumdiolate based nitrogen oxide releasing prodrugs. Three projects are described. i. Synthesis and biological evaluation of a series of new nitroxyl (HNO) releasing non-steroidal antiinflammatory drugs (NSAIDs) and comparison to related nitric oxide (NO) releasing NSAIDs A series of HNO releasing isopropylamine-based diazeniumdiolate adducts of NSAIDs and the NO releasing diethylamine diazeniumdiolate counterpart were synthesized. The aspirin derivatives were evaluated for antiinflammatory, cardioprotective and anticancer effects. Both prodrugs demonstrated similar antiinflammatory properties to aspirin but significantly lower gastrointestinal ulceration, which is a common side effect of aspirin. The HNO adduct also improved cardiac contractility. The chemotherapeutic potential of the prodrugs was assessed in vitro and in vivo. Both the prodrugs inhibited growth of cultured carcinoma cells without inducing cytotoxicity towards non-tumorogenic cell lines. The higher cytotoxicity of the HNO adduct was in part due to increased production of reactive nitrogen and oxygen species leading to oxidative damage to DNA, inhibition of glyceraldehydes-3-phosphate dehydrogenase and upregulation of signaling pathways leading to caspase-3 mediated induction of apoptosis. The NO adduct is a promising candidate for reduction of metastasis by increasing E-cadherin levels, which influences cellular adhesion. Both derivatives showed significantly reduced angiogenesis in cultured cells and tumor volume in nude mice. ii. Synthesis and characterization of primary amine based cyclic amine diazeniumdiolates and comparison to their acetoxy methyl ester derivatives. A series of HNO releasing cyclic amine diazeniumdiolates were synthesized to expand upon the few examples of primary amine diazeniumdiolates. An ester derivative of cyclopentylamine NONOate was also synthesized, to increase decomposition half-life and to improve HNO production and better cellular uptake. This modification increased its cytotoxicity compared to ionic NONOates. iii. Evaluation of mechanism of action of JS-K. JS-K (O²-(2,4-dinitrophenyl)-1-[(4-ethoxycarbonyl)-piperazin-1-yl]-diazeniumdiolate) has previously been found to be highly cytotoxic in many cancer cell lines compared to ionic diazeniumdiolates. Thus, the role of NO in cytotoxicity of JS-K was explored. A low intracellular NO flux in combination with a lack of any effect on cyclic guanosine monophosphate (cGMP) dependent pathway suggests that NO is not directly responsible for the cytotoxicity of JS-K.
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RISK FACTORS FOR PROSTATE CANCER PROGRESSIONAlgotar, Amit Mohan January 2008 (has links)
Introduction: This dissertation seeks to identify novel, potentially modifiable risk factors that could be used to reduce the risk of prostate cancer (PCa) progression. Aim 1 investigates the effects of obesity and smoking on PCa progression, aim 2 studies the effects of specific medication use on PCa progression, and aim 3 identifies factors associated with faster PCa progression.Methods: Data from 140 subjects from the Watchful Waiting study followed every 3 months for up to 5 years were used. Multiple linear regressions were used to determine associations with baseline PSA. PSA velocity (rate of change of PSA over time) was used as a surrogate marker for PCa progression. Mixed effect models were used to assess the effect of obesity, smoking and medication use on PSA velocity(aim1 and 2). For aim 3, subjects were categorized as slow, intermediate and fast progressors based on tertiles of PSA velocity. In addition to the above variables, age, Gleason score, chromogranin-A, family history, selenium and free PSA were investigated as determinants of faster PCa progression using multiple logistic regressions. Analyses were run using two models, comparing slow progressors to fast progressors (model1) and slow progressors to a combination of fast and intermediate progressors (model2).Results: Aspirin use was negatively associated with baseline PSA (coefficient = -0.39 and 95% confidence interval (CI):-0.612, -0.158). Aspirin effect was statistically significant in never smokers (coefficient = -0.54, 95% CI: -0.916, -0.170) but not in ever smokers (coefficient = -0.22, 95% CI: -0.505, 0.065). Ever smoking was statistically significantly associated with higher PSA velocity compared to never smoking (coefficient = -0.001, 95% CI: 0.0002, 0.002). In aim 3, pack-years of smoking were positively associated whereas aspirin use was negatively associated with high PSA velocity in both models. Odds Ratio and 95% CI for smoking and aspirin use for model1 and 2 respectively; 1.03 (0.92, 1.13), 1.02 (1.00, 1.03), 0.24(0.06, 0.94) and 0.26(0.10, 0.68).Conclusions: Although more studies are needed before recommendations can be made, if these results are borne to be true in other studies these modifiable risk factors can be potentially be used in prevention of PCa progression.
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Synthesis and reactivity of some novel prodrugs of anti-inflammatory agentsPowell, Sarah Llawena January 1995 (has links)
No description available.
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Comparative stability of aspirin in CSP Technologies Activ-VialTm and Owens- Illinois L-8 prescription vialsTata, Atresh, Kochak, Gregory Michael, January 2007 (has links) (PDF)
Thesis(M.S.)--Auburn University, 2007. / Abstract. Vita. Includes bibliographic references.
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An investigation into the neuroprotective properties of acetylsalicylic acid and acetaminophen /Maharaj, Himant. January 2004 (has links)
Thesis (Ph. D. (Pharmacy))--Rhodes University, 2005.
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AvaliaÃÃo do efeito terapÃutico da Aroeira-do-sertÃo (Myracrodruon urundeuva AllemÃo) na gastropatia reativa induzida por anti-inflamatÃrios nÃo esterÃides. / Evaluation of the therapeutic effect of Aroeira-do-sertÃo (Myracrodruon urundeuva AllemÃo) in the Reactive Gastropathy induced by nonsteroidal anti-inflammatory drugs.Gildo Barreira Furtado 02 October 2012 (has links)
nÃo hà / O presente ensaio clÃnico avaliou o efeito gastroprotetor do Myracrodruon
urundeuva AllemÃo (Aroeira-do-sertÃo) frente à gastropatia reativa (GR) secundÃria ao uso
oral de aspirina (Ãcido acetil salicÃlico â AAS) em baixa dose (100 mg/dia). O Myracrodruon
urundeuva AllemÃo, Ã planta nativa do Nordeste brasileiro, usada na medicina popular, como
infusos ou decoctos da entrecasca de seu tronco, para afeÃÃes dermatolÃgicas, respiratÃrias,
gastrointestinais e ginecolÃgicas. Seus extratos hidroalcÃolico e aquoso, submetidos a ensaios
farmacolÃgicos prÃ-clÃnicos, demonstraram efeitos anti-inflamatÃrio, analgÃsico, cicatrizante,
antiÃlcera, anti-histamÃnico e antibradicinÃnico e a ensaios clÃnicos preliminares, efeitos
terapÃuticos sobre Ãlceras pÃpticas e cervicites. A GR por AAS, identificÃvel e classificÃvel
endoscopicamente, foi escolhida como modelo de lesÃes gastroduodenais. Utilizou-se o elixir
de Aroeira-do-sertÃo, obtido de brotos da planta jovem. O estudo, prospectivo, randomizado,
duplo cego e comparativo com placebo, avaliou a ocorrÃncia da GR por AAS em dois grupos
de participantes tratados por 04 semanas, respectivamente com: AAS e Elixir de Aroeira
(Grupo Aroeira) e AAS e Placebo (Grupo Placebo). Antes do tratamento (prÃ-estudo), os
participantes, de ambos os sexos, com 21 a 65 anos, demonstraram normalidade
gastroduodenal por endoscopia digestiva alta (EDA); responderam a questionÃrio sobre sinais
e sintomas digestivos, com escores de frequÃncia e de intensidade, e submeteram-se a anÃlises
laboratoriais (hemograma completo, glicose, creatinina, TGO, TGP, TAP e TPTA). Doze
sujeitos incluÃram o Grupo Aroeira e 11 o Grupo Placebo. ApÃs 04 semanas, nova EDA foi
realizada, o questionÃrio sintomÃtico foi reaplicado e os exames laboratoriais foram repetidos
(pÃs-estudo). As EDAs do pÃs-estudo evidenciaram GR por AAS em 100% dos sujeitos do
Grupo Aroeira e em 82% dos sujeitos do Grupo Placebo (p = 0,2160). A anÃlise dos
questionÃrios prà e pÃs-estudo, evidenciou ausÃncia de variaÃÃes clÃnicas significantes na
comparaÃÃo intragrupo (Grupo Aroeira, p = 0,2907; Grupo Placebo, p = 0,8880) e na
comparaÃÃo intergrupo (PrÃ-estudo, p = 0,7951 vs PÃs-estudo, p = 0,6809). Em relaÃÃo aos
exames laboratoriais, apenas poucas variaÃÃes estatÃsticas em comparaÃÃes intragrupos foram
verificadas em parÃmetros do hemograma, os quais, contudo, se mantiveram nas faixas de
normalidade. TambÃm foram registradas elevaÃÃes discretas nas mÃdias das glicemias
(alteraÃÃes justificÃveis pelo perfil da populaÃÃo estudada). Estas nÃo foram estatisticamente
significantes nas comparaÃÃes prà e pÃs-estudo. Todos os demais parÃmetros laboratoriais se
mantiveram dentro das faixas de normalidade e nÃo sofreram variaÃÃes estatÃsticas
significantes nas comparaÃÃes prà e pÃs-estudo. Em conclusÃo, este estudo demonstrou que o
Myracrodruon urundeuva AllemÃo, na formulaÃÃo estudada, nÃo oferece gastroproteÃÃo
frente ao uso oral de AAS, mas tambÃm nÃo se associa a eventos adversos gastrointestinais ou
a efeitos tÃxicos hematolÃgicos ou bioquÃmicos. Em relaÃÃo ao uso de AAS em baixas doses,
o estudo demonstrou elevada incidÃncia de GR oligossintomÃtica nas semanas iniciais de
tratamento. / This clinical trial evaluated the gastroprotective effect of the Myracrodruon
urundeuva AllemÃo (Aroeira-do-sertÃo) in face of the reactive gastropathy (RG) due to the
oral usage of low-dose (100 mg/day) of aspirin (acetyl salicylic acid â ASA). The
Myracrodruon urundeuva AllemÃo, is a native plant of the Brazilian Northeast, used in
popular medicine, as infusions or decoctos of its trunk bark, for dermatologic, respiratory,
gastrointestinal and gynecologic disorders. Its hydroalcoholic and aqueous extracts were
submitted to pre-clinical pharmacologic assays which showed anti-inflammatory, analgesic,
healing, anti-ulcer, antihistaminic and antibradicininic effects. As well, preliminary clinical
assays showed its therapeutic effects to peptic ulcers and to cervicitis. The RG due to ASA,
which is identifiable and classifiable endoscopically, were chosen as gastroduodenal lesions
model. It was employed the Aroeira-do-sertÃo elixir, obtained from burgeons of the young
plant. The study was prospective, randomized, double-blind and placebo comparative and
evaluated the occurrence of RG due to ASA in 2 groups of participants treated for 4 weeks,
respectively with: ASA and Aroeira Elixir (Aroeira Group) and ASA and Placebo (Placebo
Group). Before treatments (pre-study), the participants, from both sexes, with 21 to 65 years
old, showed gastroduodenal normality by upper digestive endoscopy (UDE); answered a
digestive signs and symptoms questionnaire, with frequency and intensity scores, and
submitted to laboratory tests (CBC, Glucose, Creatinine, AST, ALT, PT and PTT). Twelve
participants were included in the Aroeira Group and 11 in the Placebo Group. After 4 weeks
of treatment, new UDEs were performed, the symptomatic questionnaire was reapplied and
the laboratory tests were repeated (post-study). The post-studies UDEs showed ASA RG in
100% of the Aroeira Group participants and in 82% of the Placebo Group participants (p =
0.2160). The pre and post-study questionnaires analysis showed no significant clinical
variations in the intragroup comparison (Aroeira Group, p = 0.2907; Placebo Group, p =
0.8880) or in the intergroup comparison (Pre-study, p = 0.7951 vs Post-study, p = 0.6809).
The laboratory tests showed a few statistically significant variations in the intragroups
comparisons of CBC parameters, which, however, stayed within the normal range values. As
well, there were discrete elevations of the medium glucose dosages (alterations justifiable by
the profile of the participantsâ population). However, these data were not statistically
significant in the pre and post-study variations comparisons. All the other laboratory
parameters stayed within the normal range values and did not show statistically significant
variations in the pre and post-study comparisons. In conclusion, this study demonstrated that
the Myracrodruon urundeuva AllemÃo, in the formulation studied, do not offer
gastroprotection to the lesions resulting by the oral ASA usage, but neither it was associated
to adverse gastrointestinal events nor to toxic hematologic or biochemical effects. In relation
to the low-dose ASA therapy, the study demonstrated a high incidence of oligosymptomatic
RG during the initial weeks of treatment.
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Avaliação farmacologica do aspirinato de atenolol como droga antiplaquetaria e anti-hipertensiva / Pharmacological evaluation of atenolol aspirinate as antiplatelet and antihypertensive drugGil, Ana Cecilia Montes 28 March 2007 (has links)
Orientador: Gilberto de Nucci / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas / Made available in DSpace on 2018-08-11T00:01:00Z (GMT). No. of bitstreams: 1
Gil_AnaCeciliaMontes_D.pdf: 1050627 bytes, checksum: 72f41a4bdcddba6633b8b082cc0ee0a0 (MD5)
Previous issue date: 2007 / Resumo: No presente trabalho, foram avaliados os efeitos farmacológicos do Aspirinato de atenolol (AA T) uma potencial pró-droga mútua resultado da combinação química entre ácido acetilsalicílico (AAS) e atenolo!. As propriedades do AA T como droga antitrombótica foram avaliadas na inibição da agregação plaquetária estimulada in vitro e na inibição da produção de tromboxano estimulada ex-vivo em sangue de animais tratados. Por outro lado, o AA T foi avaliado como droga anti-hipertensiva no modelo de hipertensão induzida pela inibição crônica da síntese de NO em ratos, e seus efeitos como antagonista dos adrenoceptores 13 foram avaliados na resposta cronotrópica ao isoproterenol em átrios isolados. Foi determinada a estabilidade metabólica em diferentes frações subcelulares hepáticas, plasma e soluções tampão de diferente pH, assim como seu perfil farmacocinético após administração endovenosa. Também foram avaliadas as propriedades ulcerogênicas gástricas e o potencial mutag'ênico através do Teste de Ames. Os resultados mostraram na avaliação do efeito antiplaquetário, que o AA T não inibiu a agregação plaquetária induzida pelo ácido araquidônico em nenhuma das concentrações testadas e apesar d~ ini~ir significativamente a produção de tromboxano estimulada ex-vivo em rat6s e na maior dose testada em camundongos, este efeito inibitório foi menor quando comparado com o AAS. O acoplamento com AAS, na molécula de AAT, suprimiu os efeitos do atenolol como antagonista dos adrenoceptores 13. Igualmente, o AA T não reduziu a freqüência cardíaca e pressão arterial após tratamento oral crônico de ratos hipertensos, estes resultados indicaram que não houve liberação de atenolol desde a molécula de AA T. Na avaliação da estabilidade metabólica e farmacocinética, observamos que o AA T seguiu uma rápida e completa hidrólise no grupo orto-acetila, gerando salicilato de atenolol (SA T), este produto foi formado quando o AA T foi submetido à hidrólise plasmática (T% 7,6 min) e aquosa (T% 56,5; 24,9 e 6,4 nos pH 2,5; 7,4 e 9.4 respectivamente) metabolização hepática e também após administração endovenosa em cães. o salicilato de atenolol formado a partir do AA T nas frações subcelulares hepáticas foi metabolizado apenas na fração microssomal gerando dois metabólitos hidroxilados em posições diferentes na molécula, a formação destes metabólitos foi dependente do tempo e paralela à cinética de desaparecimento do SAT. Após administração endovenosa, concentrações de AA T não foram detectadas em plasma. Atenolol e ácido salicílico (AS), foram liberados a partir da molécula de SAT (após clivagem da ligação éster benzoato) em concentrações significativamente menores às concentrações obtidas nos grupos tratados com AAS ou atenoloL A ASC0-24h calculada para o AS no grupo tratado com AA T correspondeu ao 0,71% da área calculada para o grupo que recebeu AAS. Similarmente, a ASC0-24h do atenolol no grupo tratado com AA T correspondeu a 1,44% da área calculada para ~ grupo tratado com atenolol. O AA T e seu principal metabólito SA T, não apresentaram propriedades mutagênicas, obtendo-se resultados negativos no Teste de Ames. O AA T produziu lesões na mucosa gástrica significativamente menores às observadas com o AAS após administração oral aguda e crônica durante 4 semanas. Devido às relevantes diferenças obtidas entre o AA T, AAS ou atenolol na caracterização farmacológica e farmacocinética, concluímos que o AA T não atua como pró-droga mútua de AAS e atenolol, e modificações futuras na molécula devem ser consideradas com a finalidade de desenvolver aspirinatos cardioativos com potencial efeito farmacológico / : In this study, we evaluated the pharmacologica/ effects of Atenolol Aspirinate (A TA) a potential mutual prodrug that resulted of the chemical combination between Acetyl Salicylic Acid (ASA) and atenolo!. The properties of ATA as anthithrombotic drug were evaluated on the inhibition of in vitro stimulated platelet aggregation and on the inhibiton of ex-vivo stimulated thromboxane production in blood from treated animais. Additionally, A TA was evaluated as an antihypertensive drug on the hypertension induced by chronic inhibition of NO in rats, its effects as antagonist of f3 adrenoceptors were evaluated in the chronotropic response to isoproterenol in isolated atria. The metabolic stability was determined in different hepatic subcellular fractions, plasma and buffer solutions as well as its pharmacokinetic profile after intravenous administration. The gastric ulcerogenic properties and mutagenic potencial, using the Ames test, were toa evaluated. In the evaluation of the antiplatelet effect, our results showed that ATA had no effect on arachidonic acid induced platelet aggregation. Although it inhibited significantly the ex-vivo stimulated thromboxane production in rats and in the highest tested dose in mice, ATA showed lower inhibitory effect than ASA. The coupling with ASA, in the ATA mOlecule, abolished the atenolol effects as antagonist of f3 adrenoceptors. In the sa~e"way, ATA had no effect reducing the heart rate and blood pressure after chropic oral treatment of hypertensive rats, these results showed that atenolol was not liberated from ATA molecule. In the evaluation of the metabolic stability and pharmacokinetics, we observed that ATA followed a rapid and complete hydrolysis at the o-acetyl group, generating atenolol salicylate (A T8), this product was formed when ATA was submitted to plasma hydro/ysis (T% 7;6 min) and aqueous hydrolysis (T% 56,5; 24,9 and 6,4 at pH 2,5; 7,4 and 9.4 respectively), hepatic metabolization and after intravenous administration to dogs. ATA was biotransformed to A TS in ali hepatic subcellular fractions, then A TS was metabolized only in the microsomal fraction generating two hydroxylated metabolites, whose formation was time dependent and parallel to the kinetics of A TS consumption. After intravenous administration, concentrations of A TS instead ATA were found in plasma dog samples, SA and atenolol were originated from cleavage of A TS molecule at the benzoate ester linkage, generating concentration levels to a lesser extent than levels found after treatment with an equimolar dose of the drugs ',nóiviõua / Doutorado / Doutor em Farmacologia
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The Role of Cyclooxygenase-2 in Newborn Hyperoxic Lung InjuryBritt, Rodney Deon, Jr. 17 December 2012 (has links)
No description available.
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Effect of Dosing Interval on the Efficacy of Misoprostol in the Prevention of Aspirin-Induced gastric Injury in the DogWard, Deborah Marie 24 April 2000 (has links)
The effect of reduced frequency of administration of misoprostol on its ability to prevent aspirin-induced gastric injury was evaluated. Twenty-four random-source dogs were divided into 4 groups which received aspirin and misoprostol as follows: Group I, 25 mg/kg aspirin PO TID and placebo PO TID; Group II, 25 mg/kg aspirin PO TID and misoprostol 3 ug/kg PO TID; Group III, 25 mg/kg aspirin PO TID, misoprostol 3 ug/kg PO BID and placebo PO QD; and Group IV, 25 mg/kg aspirin PO TID, misoprostol 3 ug/kg PO QD and placebo PO BID for 28 days. Groups were stratified to contain an equal number of dogs positive or negative for Helicobacter spp. based on results of ‘CLO test’. Gastroscopy was performed on days –9, 5, 14 and 28. Each region of the stomach was evaluated separately and visible lesions were scored on a scale of 1 (submucosal hemorrhage) to 11 (perforating ulcer). The scores for each region were summed and the median total score for each group at each day and median total score within each group between days was compared using a Kruskal-Wallis test.
No difference in total score was identified between Group I and IV on any day. Median total scores for Groups II and III were significantly(p < 0.05) lower compared to Groups I and IV on day 5. Significant difference was observed on Day 14 between the total score of Group III and Group IV. Group III had a significantly lower score (p < 0.05) than Groups I, II and IV on day 28. Gastric erosions were present in all groups in the study. This study suggests that misoprostol 3 ug/kg PO BID dosing is as effective as misoprostol 3 ug/kg PO TID dosing at preventing aspirin-induced gastric injury in this model. However, misoprostol 3 ug/kg PO TID dosing was less effective in preventing aspirin-induced gastric injury on days 14 and 28 than in previous studies. The lack of efficacy of TID dosing on days 14 and 28 may be related to higher salicylate concentrations in Group II dogs or individual variation within the small study population. / Master of Science
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