Prostaglandin E2 induces ovulation in prepubertal mice / Prostaglandina E2 induz ovulação em camundongos pré-púberes

The objective of this study was to determine the ability of prostaglandin E2 (PGE2) to induce ovulation and expression of PGE2 receptor (EP2 and EP4) and COX genes (COX-1 and COX-2) in the ovary and pituitary of prepubertal mice. The positive control consisted of the application of 5 µg of gonadotropin-releasing hormone (GnRH, n = 29); the negative control applied 0.5 mL of phosphate buffered saline (PBS, n=31); the treatment tested the application of 250 µg of PGE2 (n = 29), making a total of 89 prepubertal mice (BALB/c). Mice were euthanized 14 to 15 h after treatments to detect ovulation and tissue collection. A Chi-square test was used to compare the proportion of animals ovulating. Gene expressions and number of ovulation were analyzed by one-way ANOVA and Tukey's test was used to compare means among groups. A greater proportion of mice (P < 0.001) ovulated after receiving GnRH (89.7%, 26/29) compared to PGE2 group (58.6%, 17/29). However, the proportion was higher compared to those treated with PBS (0%, 0/31). Ep2gene expression in the pituitary was > two-fold higher (P < 0.05) in the PGE2 group compared to the PBS and GnRH groups. Further, PGE2 stimulated Cox1 (2.7 fold, P < 0.05) while GnRH stimulated Cox2 expression (6.5 fold, P < 0.05) in the pituitary when compared to the PBS group. In conclusion, our results support the hypothesis that PGE2 can induce ovulation in prepubertal mice with a concomitant increase in Ep2 and Cox1 gene expression in the pituitary gland.(AU)

O objetivo deste estudo foi determinar a capacidade da prostaglandina E2 (PGE2) em induzir a ovulação e expressão do receptor PGE2 (EP2 e EP4) e genes COX (COX-1 e COX-2) no ovário e na hipófise de camundongos pré-púberes. O controle positivo consistiu na aplicação de 5 µg de hormônio liberador de gonadotrofina (GnRH, n = 29); o controle negativo aplicação 0,5 mL de tampão fosfato-salino (PBS, n=31); o tratamento testado aplicação de 250 µg de PGE2 (n = 29), perfazendo um total de 89 camundongos (BALB/c) pré-púberes. Os camundongos foram sacrificados 14 a 15 h após os tratamentos para detectar ovulações e coleta de tecido. O teste do qui-quadrado foi usado para comparar a proporção de animais ovulando. As expressões gênicas e o número de ovulação foram analisados por ANOVA e o teste de tukey foi usado para comparar as médias entre os grupos. Uma maior proporção de camundongos (P <0,001) ovulou após receber GnRH (89,7%, 26/29) em comparação com o grupo PGE2 (58,6%, 17/29). No entanto, a proporção foi maior em comparação com aqueles tratados com PBS (0%, 0/31). A expressão do gene Ep2 na hipófise foi duas vezes maior (P <0,05) no grupo PGE2 em comparação com os grupos PBS e GnRH. Além disso, a PGE2 estimulou a Cox1(2,7 vezes, P <0,05) enquanto o GnRH estimulou a expressão de Cox2 (6,5 vezes, P <0,05) na pituitária em comparação com o grupo PBS. Em conclusão, nossos resultados suportam a hipótese de que PGE2 é capaz de induzir ovulação em camundongos pré-púberes com aumento concomitante na expressão dos genes Ep2 e Cox1 na glândula pituitária.(AU)

Root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin E 2 and leukotriene B 4 signaling in apical periodontitis

Abstract Purpose To evaluate the kinetics of apical periodontitis development in vivo , induced either by contamination of the root canals by microorganisms from the oral cavity or by inoculation of bacterial lipopolysaccharide (LPS) and the regulation of major enzymes and receptors involved in the arachidonic acid metabolism. Methodology Apical periodontitis was induced in C57BL6 mice (n=96), by root canal exposure to oral cavity (n=48 teeth) or inoculation of LPS (10 µL of a suspension of 0.1 µg/µL) from E. coli into the root canals (n= 48 teeth). Healthy teeth were used as control (n=48 teeth). After 7, 14, 21 and 28 days the animals were euthanized and tissues removed for histopathological and qRT-PCR analyses. Histological analysis data were analyzed using two-way ANOVA followed by Sidak's test, and qRT-PCR data using two-way ANOVA followed by Tukey's test (α=0.05). Results Contamination by microorganisms led to the development of apical periodontitis, characterized by the recruitment of inflammatory cells and bone tissue resorption, whereas inoculation of LPS induced inflammatory cells recruitment without bone resorption. Both stimuli induced mRNA expression for cyclooxygenase-2 and 5-lipoxygenase enzymes. Expression of prostaglandin E 2 and leukotriene B 4 cell surface receptors were more stimulated by LPS. Regarding nuclear peroxisome proliferator-activated receptors (PPAR), oral contamination induced the synthesis of mRNA for PPARδ, differently from inoculation of LPS, that induced PPARα and PPARγ expression. Conclusions Contamination of the root canals by microorganisms from oral cavity induced the development of apical periodontitis differently than by inoculation with LPS, characterized by less bone loss than the first model. Regardless of the model used, it was found a local increase in the synthesis of mRNA for the enzymes 5-lipoxygenase and cyclooxygenase-2 of the arachidonic acid metabolism, as well as in the surface and nuclear receptors for the lipid mediators prostaglandin E2 and leukotriene B4.

Effects of morphine on the expression of cytokines and inflammatory mediators in a rabbit model of endotoxin-induced experimental uveitis / Efeitos da morfina na expressão de citocinas e de mediadores inflamatórios em coelhos com uveítes experimental induzida por endotoxina

ABSTRACT Purpose: To evaluate the effects of 1% morphine instillation on clinical parameters, aqueous humor turbidity, and expression levels of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1beta), prostaglandin E2 (PGE2), and myeloperoxidase (MPO) in rabbits with endotoxin-induced experimental uveitis. Methods: Twenty four New Zealand white rabbits were divided into four groups (n=6 each): control (CG), morphine (MG), naloxone (NG), and morphine-naloxone (MNG) groups. Under dissociative anesthesia, 0.1 mL of solution containing 0.2 µg of lipopolysaccharide (LPS) endotoxin from the Salmonella typhimurium cell wall was injected in the vitreous chamber. Clinical evaluations (conjunctical hyperemia, chemosis blepharospasm, and ocular discharge) and laser flaremetry were performed before (baseline), and 10 and 20 hours after induction of uveitis. Rabbits were subsequently euthanized and eyes were enucleated to quantify expression levels of TNF-α, IL-1 beta, PGE2, and MPO. Results: No significant differences in clinical parameters and flare values were observed between the study groups. TNF-α and IL-1 beta levels increased significantly in the CG, MG, NG, and MNG groups compared to baseline (P<0.05). Significant differences in PGE2 levels were observed between the MG and NMG groups (P<0.05). A trend toward increased MPO activity was observed in response to uveitis induction; however, this trend did not reach statistical significance (P>0.05). Conclusions: Morphine has no effect on clinical parameters, flare, or expression levels of inflammatory mediators in a rabbit model of uveitis induced by intravitreal injection of LPS.

RESUMO Objetivo: Estudaram-se os efeitos da instilação de morfina 1% sobre parâmetros clínicos, turbidez do humor aquoso e expressão de fator de necrose tumoral alfa (TNF-alfa), de interleucina-1 beta (IL-1beta), de prostaglandina E2 (PGE2) e de mieloperoxidase (MPO), em olhos de coelhos com uveíte induzida por endotoxina. Material e Métodos: Vinte e quatro coelhos da raça Nova Zelândia Branco foram distribuídos em quatro grupos (n=6, em cada): grupo controle (GC), morfina (GM), naloxona (GN) e morfina-naloxona (GMN). Sob anestesia dissociativa, injetou-se 0,1 mL de solução contendo 0,2 µg de lipossacarídeo (LPS) endotóxico da parede celular de Salmonella typhimurium na câmara vítrea. Realizou-se avaliação clínica (hiperemia conjuntival, quemose, blefaroespasmo e secreção ocular) e a flaremetria a “laser” antes (basal) e após 10 e 20 horas da indução da uveíte. No final, os coelhos foram submetidos à eutanásia e os olhos com uveíte foram enucleados para a quantificação dos níveis de TNF-alfa, IL-1 beta, PGE2 e MPO. Diferenças foram consideradas significativas quando p<0,05. Resultados: Os grupos da pesquisa não diferiram quanto aos parâmetros clínicos e os valores de “flare”. Observou-se elevação significativa nos níveis de TNF-alfa e de IL-1 beta, comparativamente ao basal, nos grupos GC, GM, GN e GMN (p<0,05). Valores de PGE2 variaram entre os grupos GM e GNM (p<0,05). A atividade de MPO aumentou após a indução da uveíte, porém, sem significância estatística (p>0,05). Conclusões: A morfina não atuou sobre parâmetros clínicos, “flare” e expressão dos mediadores inflamatórios estudados, quando instilada em olhos de coelhos com uveíte induzida por injeção intravítrea de LPS.

Possible roles of COX-1 in learning and memory impairment induced by traumatic brain injury in mice

People who suffer from traumatic brain injury (TBI) often experience cognitive deficits in spatial reference and working memory. The possible roles of cyclooxygenase-1 (COX-1) in learning and memory impairment in mice with TBI are far from well known. Adult mice subjected to TBI were treated with the COX-1 selective inhibitor SC560. Performance in the open field and on the beam walk was then used to assess motor and behavioral function 1, 3, 7, 14, and 21 days following injury. Acquisition of spatial learning and memory retention was assessed using the Morris water maze on day 15 post-TBI. The expressions of COX-1, prostaglandin E2 (PGE2), interleukin (IL)-6, brain-derived neurotrophic factor (BDNF), platelet-derived growth factor BB (PDGF-BB), synapsin-I, and synaptophysin were detected in TBI mice. Administration of SC560 improved performance of beam walk tasks as well as spatial learning and memory after TBI. SC560 also reduced expressions of inflammatory markers IL-6 and PGE2, and reversed the expressions of COX-1, BDNF, PDGF-BB, synapsin-I, and synaptophysin in TBI mice. The present findings demonstrated that COX-1 might play an important role in cognitive deficits after TBI and that selective COX-1 inhibition should be further investigated as a potential therapeutic approach for TBI.

Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine

Candida albicans utilizes arachidonic acid (AA) released during the course of infection (Candidiasis) from phospholipids of infected host cell membranes and synthesizes extracellular prostaglandin(s) which play an important role in hyphae formation and host cell damage. C. albicans biofilms secrete significantly more prostaglandin(s) and evidence suggests that Candida biofilms have dramatically reduced susceptibility to majority of antifungal drugs. AA influences the saturation level of lipids and fluidity of yeast cell membranes. Therefore the aim of this study was to evaluate the effect of AA alone or in combination with antifungal agents on biofilm formation and production of prostaglandin (PGE2) in C. albicans, C. parapsilosis, C. glabrata, C. tropicalis, and C. albicans amphotericin B resistant strain (AmBR). Maximum biofilm formation was found to be in the case of C. albicans compared to C. non-albicans species. However, among the non-albicans species C. tropicalis exhibited highest biofilm formation. Treatment with AA in combination with subinhibitory concentrations of fluconazole and terbinafine separately exhibited significant (p < 0.05) reduction in biofilm formation against C. glabrata, C. parapsilosis, C. tropicalis and AmBR as compared to their individual effect. Further, these two antifungal agents in combination with AA caused an increase in production of prostaglandin from fungal cell itself which was significant (p < 0.05) in case of all the strains tested.

In vivo and in vitro anti-inflammatory activity of Cryptostegia grandiflora Roxb. ex R. Br. leaves

BACKGROUND: Despite Cryptostegia grandiflora Roxb. ex R. Br. (Apocynaceae) leaves are widely used in folk Caribbean Colombian medicine for their anti-inflammatory effects, there are no studies that support this traditional use. Therefore, this work aimed to evaluate the effect of the total extract and primary fractions obtained from Cryptostegia grandiflora leaves, using in vivo and in vitromodels of inflammation, and further get new insights on the mechanisms involved in this activity. RESULTS: Ethanolic extract of Cryptostegia grandiflora leaves, and its corresponding ether and dichloromethane fractions, significantly reduced inflammation and myeloperoxidase activity (MPO) in ear tissue of mice treated with 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Histological analysis revealed a reduction of edema and leukocyte infiltration. Complementarily, we demonstrated that extract and fractions reduced nitric oxide (NO•) and prostaglandin E2 (PGE2) production in LPS-stimulated RAW 264.7 macrophages, as well as scavenging activity on DPPH and ABTS radicals. CONCLUSIONS: Our results demonstrated for the first time the anti-inflammatory activity of Cryptostegia grandiflora leaves, supporting its traditional use. This activity was related to inhibition of MPO activity, and PGE2 and NO• production. These mechanisms and its antioxidant activity could contribute, at least in part, to the anti-inflammatory effect showed by this plant.

Preventive effect of Ligularia fischeri on inhibition of nitric oxide in lipopolysaccharide-stimulated RAW 264. 7 macrophages depending on cooking method

BACKGROUND: Ligularia fischeri (common name Gomchwi) is known for its pharmaceutical properties and used in the treatment of jaundice, scarlet-fever, rheumatoidal arthritis, and hepatic diseases; however, little is known about its anti-inflammatory effect. In this study the influence of blanching and pan-frying on the anti-inflammatory activity of Ligularia fischeri (LF) was evaluated. RESULTS: Fresh LF and cooked LF showed no significant effect on the viability of macrophages after 24 h incubation. Fresh LF was found to be the most potent inhibitor of nitric oxide (NO) production at 100 µg/ml, while pan-fried LF showed little inhibitory effect on lipoloysaccharide (LPS) stimulated murine machrophage RAW264.7 cells. In contrast with its effect on NO production, pan-fried LF showed significant attenuation of the expression of inducible nitiric oxide synthase (iNOS) compared with fresh LF. In the cooking method of LF, PGE2 production was not affected in the LPS-induced RAW 264.7 cells. In LPS-induced RAW 264.7 cells, pretreatment by fresh and cooked LF increased COX2 mRNA expression. The 3-O-caffeoylquinic acid content of blanching and pan-frying LF increased by 4.92 and 9.7 fold with blanching and pan-frying respectively in comparison with uncooked LF. CONCLUSIONS: Regardless of the cooking method, Ligularia fischeri exhibited potent inhibition of NO production through expression of iNOS in LPS-induced RAW264.7 cells.

Association between gingival crevicular fluid prostaglandin E 2 level and preterm low birth weight.

Background: Periodontal infections, which serve as a reservoir of inflammatory mediators such prostaglandin E 2 (PGE 2 ), may pose a threat to the fetal-placental unit and cause preterm delivery. Aim: This study was conducted to estimate the PGE 2 levels in gingival crevicular fluid (GCF) and to explore the association between GCF-PGE 2 levels and preterm low birth weight (PLBW). Materials and Methods: Twenty-two pregnant patients were selected for the study. GCF samples were collected from these patients before delivery and again at 1 month after delivery. PGE 2 level was estimated using a commercially available ELISA kit (Neogen™). Results: The mean GCF-PGE 2 level was 5.8 ng/ml before parturition and 5.5 ng/ml after parturition, but the difference was not statistically significant. There was negative correlation between PGE 2 levels and gestational age at birth. Conclusion: The study provides weak evidence that there is correlation between GCF-PGE 2 levels and birth outcome. Further clinical trials with large samples are required to confirm the association between GCF-PGE 2 levels and PLBW.

Efecto antiinflamatorio de apitoxina de Apis mellifera sobre prostaglandina E2 del fluido crevicular gingival de pacientes con y sin enfermedad periodontal, sometidos a apiterapia: ensayo preliminar / Anti-inflammatory effect of apitoxin and Apis mellifera on prostaglandin E2 in gingival crevicular fluid of patients with and without periodontal disease, submitted to apitherapy: preliminary test

Introducción: La apitoxina que es producida por la Apis mellifera posee efecto antiinflamatorio sobre una serie de marcadores biológicos. La prostaglandina E2 forma parte de ellos, estando presente en el fluido gingival crevicular (FGC). La prostaglandina E2 es evidenciada en la enfermedad periodontal. Objetivo: En este estudio se evaluó el efecto antiinflamatorio de la apitoxina sobre la concentración de prostaglandina E2 del FGC de un paciente sin enfermedad periodontal (SEP) y otro con enfermedad periodontal (CEP). Materiales y Método: Se seleccionó un paciente SEP y otro CEP, que sometidos a apiterapia durante 28 días, se registraron 5 muestras por paciente de FGC, siendo almacenadas, centrifugadas y refrigeradas para su conservación. Posteriormente se midió la concentración de prostaglandina E2 crevicular mediante inmunodifusión radial simple en placas petri con concentración de anticuerpo anti prostaglandina E2 de 1:1000. Selladas a 4°C, se esperó 72 horas para permitir su difusión, tiñéndose con Azul brillante de Coomasie, determinándose la concentración de cada placa. Resultados: Paciente SEP inmediatamente antes de apiterapia presentó una concentración de 0.9636 ± 0.0055 (ug/uL), finalizando con una concentración de 0.9196+/-0.0733 (ug/uL) al completar 28 días de tratamiento. El paciente CEP antes de recibir apiterapia presento una concentración de 1.1866 +/- 0.0867 (ug/uL), finalizando con una concentración de 0.9858 +/- 0.0074 (ug/uL) al completar 28 días de tratamiento. Discusión: Los hallazgos de este estudio demuestran una disminución de la concentración de PGE2 del FGC tanto para el paciente CEP y SEP sometidos a apiterapia durante 28 días, siendo esta disminución 3.7 veces mayor en el paciente CEP.

Introduction: Apitoxin, which is produced by Apis mellifera, has anti-inflammatory effect on a number of biomarkers. Prostaglandin E2 is one of them, being present in gingival crevicular fluid (GCF). Prostaglandin E2 is evidenced in periodontal disease. Objective: This study evaluated the antiinflammatory effect of apitoxin on concentration of prostaglandin E2 FGC in a patient with no periodontal disease (SEP) and other with periodontal disease (CEP). Materials and Methods: We selected both a SEP and CEP patient who were subjected to apitherapy for 28 days. There were 5 samples per patient of FGC, being stored, centrifuged and refrigerated for their preservation. Subsequently, the concentrations of crevicular prostaglandin E2 were measured by simple radial immunodiffusion in petri dishes with antibody concentration of prostaglandin E2 of 1:1000. Sealed at 4 °C, after 72 hours to allow diffusion, they were stained with Coomassie Brilliant Blue, determining the concentration of each plate. Results: SEP patient immediately before apitherapy presented a concentration of 0.9636 +/- 0.0055 (g / mL), ending with a concentration of 0.9196 +/- 0.0733 (g / mL) upon completion of 28 days of treatment. CEP patient before receiving apitherapy showed a concentration of 1.1866 +/- 0.0867 (g/mL), ending with a concentration of 0.9858 +/- 0.0074 (g/mL) upon completion of 28 days of treatment. Discussion: The findings of this study show a decrease in the concentration of PGE2 of FGC both for the CEP and SEP patient subjected to apitherapy for 28 days, being this decrease 3.7 times higher in the CEP patient.

Effects of carprofen administered by different routes to control experimental uveitis in dogs / Efeitos do carprofeno, aplicado por diferentes vias, no controle de uveítes experimentais em cães

Efficacy of carprofen, administered by different routes, was studied in experimental uveitis in dogs. Anterior chamber paracenteses was accomplished at two different moments (M0 and M1), with a five hour interval between them. At M0 and M1, 0.2mL of aqueous humor was collected and quantitation of total protein and prostaglandin E2 (PGE2) were determined. Four groups were formed (n=8), which received carprofen at the end of M0, by the following routes: subcutaneous (GIm), subconjunctival (GII), and topical (GIII). A fourth group that received no treatment was instituted (Control). Conjunctival histopathology of the GII animals was performed. In all groups, values of protein and PGE2 significantly enhanced at M1; however, they did not significantly change among groups at M1. Inflammatory exudate of acute character and mild hemorrhage were seen at histopathology after carprofen administration. Carprofen was unable to inhibit PGE2 synthesis and the protein influx to the anterior chamber by any of the tested routes. However, the reduction of 44 percent in protein levels (topical) suggests that the agent can be used by this route as an adjuvant to control uveitis in dogs.

Estudaram-se os efeitos do carprofeno, aplicado por diferentes vias, em uveítes experimentais em cães. Realizou-se paracentese de câmara anterior em dois momentos (M0 e M1), com intervalo de cinco horas entre si. Em M0 e M1, colheram-se 0,2mL de humor aquoso e determinaram-se as concentrações de proteína total e de prostaglandina E2 (PGE2). Constituíram-se quatro grupos (n = 8), que receberam carprofeno ao final de M0 pelas vias subcutânea (GI), subconjuntival (GII) e tópica (GIII). Um quarto grupo não recebeu tratamento (controle). Procedeu-se à avaliação histopatológica nos indivíduos do GII. Em todos os grupos, encontrou-se aumento significativo dos níveis proteicos e de PGE2 em M1. Não se observou diferença significativa, em M1, entre os grupos para nenhum dos parâmetros estudados. Exsudado inflamatório de caráter agudo e hemorragia discreta foram vistos à histopatologia após a aplicação do fármaco. O carprofeno foi ineficaz em inibir a síntese de PGE2 e o influxo de proteínas para a câmara anterior, por qualquer uma das vias testadas. Contudo, a redução de 44 por cento nos níveis de proteínas (via tópica), sugere que por esta via ele pode ser utilizado como adjuvante no controle da uveíte em cães.

Juveniles versus adults: differences in PGE2 levels in the gingival crevicular fluid during orthodontic tooth movement

This study aimed to investigate age-related changes in the biosynthetic capacity of prostaglandin E2 (PGE2) in the gingival crevicular fluid (GCF) during one month of orthodontic treatment. Twenty-five juvenile subjects (mean age 13 ± 2.1 years) and 23 adults (mean age 24 ± 2.1 years) were included. GCF was collected immediately before the force application at the baseline, 2, 21 and 28 days, with periopaper inserted into the gingival crevice of the maxillary lateral incisors. The mediator levels were determined with an EIA kit. The results showed that the PGE2 concentrations were significantly elevated from the baseline to 21 days (129.35 and 198.84 pg/µL, p = 0.0169) in juvenile subjects and reduced from 21 to 28 days (198.84 to 112.60 pg/µL, p = 0.0032). Adults, however, had no significant changes in the PGE2 levels. The total amounts of PGE2 from both groups changed between the baseline to 21 and 21 to 28 days (p = 0.0119 and p = 0.0076, respectively). The PGE2 initial and final levels showed significant differences between the juveniles and adults, being higher in adults (baseline: juvenile = 129.35 pg/µL vs. adult = 163.20 pg/µL, p = 0.0379; t3: juvenile = 112.60 pg/µL and adult = 175.30 pg/µL, p = 0.0005). In conclusion, the results demonstrate the presence of variation in the PGE2 levels according to age and the orthodontic activation period, which can explain why the speed of orthodontics treatment may be different in adults vs. juveniles.

Interleukin-1beta stimulates matrix metalloproteinase-2 expression via a prostaglandin E2-dependent mechanism in human chondrocytes

IL-1beta is known promote cyclooxygenase-2 (COX- 2) and matrix metalloproteinase-2 (MMP-2) expression. This study focuses on the characterization of the signaling cascade associated with IL-1beta-induced matrix metalloproteinase-2 (MMP- 2) regulation in human chondrocytes. The decrease in collagen levels in the conditioned media was prevented by a broad spectrum MMP inhibitor, suggesting that IL-1beta promotes the proteolytic process leading to MMP-2 activation. IL-1beta-related MMP-2 expression was found to be dependent on prostaglandin E2 (PGE2) production. In addition, the induction of COX-2 and MMP-2 was inhibited by the pretreatment of chondrocytes with a SB203580 or Ro 31-8220, indicating the involvement of protein kinase C (PKC) or p38 mitogen-activated protein kinase (MAPK). However, there is no cross-talk between PKC and p38 MAPK in the IL-1beta-induced MMP-2 activation. Taken together, these results demonstrated that IL-1beta induces MMP-2 expression through the PGE2-dependent mechanism in human chondrocytes.

Subcellular distribution of prostaglandin-E2 and prostaglandin-F2alpha in atrial tissue from patients with mitral valve disease

The distribution of prostaglandin-E2 (PGE2) and prostaglandin-F2alpha (PGF2alpha) was studied in subcellular fractions isolated from homogenates of human atrial fresh tissue by differential centrifugation. Right and left atrial samples were excised from the same heart of six patients with mitral valve disease at the time of open heart surgery. The atrial fractions investigated were mitochondrial (8,500 g pellet), microsomal (100,000 g pellet) and cytosol soluble (100,000 g supernatant) fractions. After extraction of prostaglandins from the three atrial fractions and separation of PGE from PGF series by chromatography on silicic acid column, these prostaglandins were measured by radioimmunoassay. The results, showed that PGE2 and PGF2alpha were located mainly in the soluble cytosolic fraction of right and left atrial tissue (p<0.001). Furthermore, the prostaglandins levels were higher in left than in right atria of these patients (p<0.001). The relation between prostaglandins heart generation in response to elevated work load of mitral valve disease is discussed.

Compresión epidural neoplásica. Nuevas alternativas terapéuticas / Neoplastic spinal cord compression. New therapeutic alternatives

La compresión epidural neoplásica (CEN) es una complicación frecuente en pacientes oncológicos, la fisiopatología del mismo es poco comprendida y generalmente relacionada a un efecto mecánico: el tratamiento convencional incluye la utilización de corticoides y radioterapia. Se han demostrado tres nuevos aspectos en la fisiopatología de la CEN: 1) El rol protagónico de la prostaglandina E2 (PGE2) en el incremento de la permeabilidad vascular y la formación del edema de tipo vasogénico. 2) El neurotrasmisor serotonina que actúa estimulando tanto la producción de PGE2 como la acción neurotóxica de los aminoácidos exitatorios. 3) La acción de las exitotoxinas en el daño tisular neural secundario a la alteración del flujo de sodio, cloro y calcio. Estos tres aspectos fisiopatológicos tienen su respaldo en 1) Indometacina como inhibidor de la producción de PG. 2) Ciproheptadina, p-clorofenilalanina y ketanserina como antiserotoninérgicos. 3) MK-801 y ketamina como antagonistas del glutamato. El uso racional de estos fármacos pueden contribuir a retardar la instalación del cuadro neurológico permitiendo la mejor utilización de terapias más definitivas

Estimation of prostaglandin E2 and 6-Keto-prostaglandin F1 in cases of chronic tonsillitis

This study was carried out on 50 patients suffering from chronic tonsillitis of different age groups. Prostagl and in E2 and 6-ketoprostagl and in F1 were estimated in the tissue of tonsils by radioimmunoassay methods. It was concluded that the young age groups [4 - 7 years] had higher levels of prostagl and in E2 and 6-ketoprostagl and in F1. The young age groups [4 - 7 years and 8 - 12 years] had higher levels of prostagl and in E2 more than 6-ketoprostagl and in F1, the older age group [13 - 18 years] had higher levels of 6-ketoprostagl and in F1 than prostagl and in E2. The levels of prostagl and in E2 were higher than the levels of 6-ketoprostagl and in F1 in the tissues of tonsils; while in plasma 6-ketoprostagl and in, F1 was higher than prostagl and in E2. Prostagl and in E2 was secreted from lymphocytes of tonsils

Arachidonic acid and prostaglandin E2 in allergic nasal tissues

This study was carried out on 60 persons, 40 of them were suffering from allergic rhinitis, while 20 were normal [control group]. Arachidonic acid and PGE2 levels were estimated in the nasal tissues by gas chromatography and radioimmunoassay methods. There was a marked increase in arachidonic acid and PGE2 levels in nasal tissues in cases of allergic rhinitis. There was significant positive correlation between arachidonic acid and PGE2 [r = 0.92]. In the allergic group, there was no sex variation in arachidonic acid and PGE2 levels. The increase in both arachidonic acid and PGE2 in nasal tissues of allergic rhinitis patients was explained by excessive nasal tissue uptake of arachidonic acid or excessive synthesis from linoleic acid, but not due to the decrease in the degradation of PGE2. These findings can help in the study and management of allergic rhinitis

Comportamiento de los niveles de prostaglandina E2 y prostaciclina (PGI2) en la mucosa gástrica de ratas dañadas por etanol y estrés / Behavior of prostaglandin E2 and prostacycline (PGI2) levels in the gastric mucosa of rats damaged by ethanol and stress

Las prostaglandinas protegen la mucosa gastrointestinal contra varios agentes ulcerógenos. Existen pocos reportes acerca de los niveles de prostaglandinas endógenas en la mucosa gástrica dañada por diferentes modelos de producción de lesiones gástricas. Presentamos un estudio sobre los efectos del etanol y del estrés por inmovilización más frío, sobre los niveles de prostaglandina E2 y prostaciclina en la mucosa gástrica de ratas. Como controles se usaron ratas intactas. Los niveles mucosales de ambos prostanoides se determinaron por radio-inmunoensayo. Obtuvimos como resultados que la concentración de prostaglandina E2 sufrió un discreto aumento en el modelo de estrés y una disminución significativa en las ratas tratadas con etanol. La concentración de prostaciclina se comportó de manera exactamente contraria, presentó una disminución significativa en el modelo de estrés y un aumento discreto en el modelo de etanol. Este comportamiento puede deberse a una diferencia en la fisiopatología de ambos modelos experimentales

Prostaglandina E2 (PgE2) en encía normal e inflamada: ensayo clínico; revisión bibliográfica / Prostaglandin E2 (PgE2) in normal and inflamed gingiva: clinical assay; bibliographic review

Se analiza el papel de las prostagladinas (Pg) en la patogenia de la enfermedad parodontal, para lo cual se tomaron 92 muestras de encías a igual nùmero de pacientes (48 femeninos y 44 masculinos) cuyas edades oscilaron entre 17 y 74 años de edad. Se clasificaron clìnicamente segùn el índice gingival de Löe. La presencia de prostaglandina se realizó según el método de cromatografía en capa delgada. Se relacionó la presencia o ausencia de PgE2 con el sexo, edad, índice gingival de Löe y el grado de infiltrado inflamatorio. Encontramos que aunque la correlación entre el índice gingival de Löe con el grado de infiltrado inflamatorio no se corresponden exactamente, el primero brinda una útil orientación clínica inicial. En los pacientes con mayor grado de inflamación se correspondieron mayores concentraciones de PgE. Se plantea la posibilidad del uso de drogas inhibidoras de prostaglandina en el tratamiento de la enfermedad parodontal