Biochemical and immunohistochemical examination of the effects of ephedrine in rat ovary tissue

Purpose: It was aimed to investigate the biochemical and immunohistochemical effects of ephedrine (EPH) in bilateral ovariectomized rats. Methods: Twenty-four Sprague Dawley female rats were divided into three groups: control group: The abdomen was opened and closed without any treatment; ischemia-reperfusion (IR) group: 2 h of ischemia followed by 2 h of reperfusion were allowed to cause IR injury; IR+EPH group: oral EPH solution (5 mg/kg) was administered for 28 days. Results: Biochemical parameters were statistically significant in group comparisons. Increased interleukin-6 (IL-6) expression, degenerative preantral and antral follicle cells and inflammatory cells around blood vessels were seen in IR group. Negative IL-6 expression was observed in seminal epithelial cells, preantral and antral follicle cells in IR+EPH group. While caspase-3 activity increased in granulosa cells and stromal cells in IR group, caspase-3 expression was negative in preantral and antral follicle cells in the germinal epithelium and cortex in IR+EPH group. Conclusion: The effect of apoptosis, which occurs with the signaling that starts in the cell nucleus, caused the cessation of the stimulating effect at the nuclear level after EPH administration, and a decrease in the antioxidative effect in IR damage and inflammation in the apoptotic process.

The role of visfatin levels in gingival crevicular fluid as a potential biomarker in the relationship between obesity and periodontal disease

Abstract Objectives Visfatin is an adipokine that plays an important role in immune functions as a growth factor, enzyme, and pro-inflammatory mediator. We aimed to determine the levels of visfatin, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in gingival crevicular fluid (GCF) in both obese/non-obese patients, with/without generalized chronic periodontitis (GCP). Methodology Patients were categorized as obese (O) (n=31) or non-obese (nO) (n=19). Groups were divided into four subgroups according to periodontal conditions: (1) periodontally healthy without obesity (nO-Ctrl); (2) GCP without obesity (nO-CP); (3) periodontally healthy with obesity (O-Ctrl); and (4) GCP with obesity (O-CP). Demographic variables, anthropometric and laboratory data were recorded. Periodontal parameters were measured at baseline and 3rd months after either non-surgical periodontal treatment or calorie -restricted diet therapy. At the same time, GCF samples were taken from patients to analyze TNF-alpha, IL-6,and visfatin levels. Results Periodontal parameters were significantly higher in the O group than in the nO group (P<0.05). IL-6 levels were higher in the O group than in the nO group (P<0.001). The visfatin levels of the obese patients were reduceddecreased following the treatments (P<0.05). Cholesterol levels were higher in the O group than in the nO groups (P<0.05). IL-6 levels were higher in O-CP and O-Ctrl groups than in the nO-Ctrl group (P<0.05). Compared to the other groups, visfatin levels were significantly higher in the O-CP group but decreased following treatment (P<0.05). Conclusions Our findings suggest that visfatin and IL-6 levels in GCF are associated with the pathogenesis of obesity and periodontitis. Within the limits of this study, we considered that there might be an association between the lipid profile and periodontitis on systemically healthy individuals.

Kinetin inhibits apoptosis of aging spleen cells induced by D-galactose in rats

Kinetin (Kn) is a cytokinin growth factor that exerts several anti-aging and antioxidant effects on cells and organs. To investigate the mechanism underlying apoptotic events in aging cells induced by D-galactose (D-gal), we examined the effect of Kn delivered via nuchal subcutaneous injection on D-gal-induced aging and apoptosis in rats. Our results showed that interleukin (IL)-2 levels and mitochondrial membrane potential (DeltaPsim) were decreased by Kn in aging rats while IL-6 production and apoptosis increased. In addition, the expression of anti-apoptotic Bcl-2 was low while that of Bax was high in the aging group. After treated with Kn, compared with aging group, there showed obvious difference in Kn group with elevated IL-2, proliferation index, Bcl-2, DeltaPsim and decreased IL-6 and Bax in splenic lymphocyte. Based on these results, we concluded that Kn can effectively protect the rat spleen from aging, apoptosis, and atrophy.

Renal cell carcinoma and systemic onset juvenile idiopathic arthritis.

Renal cell carcinoma (RCC) accounts for majority of malignancies arising out of the kidney. Paraneoplastic rheumatologic manifestations; myositis, vasculitis, and arthritis have been described in a few cases with RCC. Systemic onset juvenile idiopathic arthritis (JIA) is characterized by intermittent fever, arthritis, reticulo-endothelial cell hyperplasia and absence of rheumatoid factor and antinuclear antibodies. Herein, we report a 16-year-old boy with systemic onset JIA for 5 years who developed RCC and his systemic and articular symptoms paralleled the course of RCC. The common pathophysiologic influence of the cytokine Interleukin-6 possibly played a role in the exacerbation of symptoms of systemic onset JIA during the relapse of the RCC. The case is presented to highlight the rare co-occurrence of these two diseases and their influence on each other.

Fisiopatologia da osteoporose involutiva / Physiopathology of involutive osteoporosis

A diminuição da densidade mineral óssea (DMO) com a idade é um fenômeno universal, atingindo todas as raças e culturas, não patológico em si, mas que se constitui um substrato para o desenvolvimento da osteoporose (OP). Em 1941, Albright descreveu pela primeira vez a OP, e chamou atenção para deficiência de estrógeno (E2) como causa principal desta patologia. Isso foi confirmado em trabalho posteriores, onde a reposição hormonal preveniu a perda óssea. Posteriormente, Riggs e Melton classificaram a OP involutiva em tipo I e tipo II. A OP tipo I, ou pós-menopáusica, ocorre nos 10 anos que se seguem à menopausa, sendo uma conseqüência da deficiência de E2. Porém, o mecanismo de ação do E2 no osso ainda é desconhecido. Vários trabalhos não evidenciaram receptores de E2 em osteoclastos, sugerindo que o efeito do E2 se faz de forma indireta via osteoblastos ou pelas células do estroma da medula óssea, através da liberação de mediadores. Dados recentes controversos sobre o papel da interleucina 6 como mediadora do efeito estrogênico. A OP tipo II, ou senil, ocorreria após 65 anos. À partir dessa idade, outros fatores também seriam determinantes da OP, dentre eles o hiperparatiroidismo secundário. Recentemente, Riggs e Melton retornaram a teoria unitária do modelo de OP involutiva, colocando o E2 como fator etiológico central para ambas as fases de perda óssea. As discussões sobre as classificações da OP têm objetivos didáticos, mas demonstram também o caráter heterogêneo e multifatorial da doença.

The induction of cyclooxygenase-2 (COX-2) in cultured endothelial cells treated with serum from preeclampsia is mediated by interleukin-6.

COX-2 protein, but not COX-1 protein, was induced in HUVEC from women with a normal pregnancy (nHUVEC) treated with serum from patients with preeclampsia (pSerum), but not with serum from women with a normal pregnancy (nSerum). COX activity in pSerum treated nHUVEC was less than in nSerum treated nHUVEC. Interestingly, the induction of COX-2 protein in nHUVEC treated with pSerum was inhibited by antiIL-6 antibody. The decreased COX activity in nHUVEC treated with pSerum plus antiIL-6 antibody was also reversed in a dose dependent manner. Thus, the induction of COX-2 in pSerum treated nHUVEC was mediated by IL-6. Therefore, the development of selective inhibitors of COX-2 or of IL-6 antagonists may have a potential role in the prevention and treatment of preeclampsia.

Increased pro-inflammatory cytokines (TNF-[alfa] and IL-6) and anti-inflammatory compounds (sTNFRp55 and sTNFRp75) in brazilian patients during exanthematic dengue fever

Pro-inflammatory cytokines, tumor necrosis factor (TNF-[alfa]), interleukin-6(IL-6) and interleukin-1ß (IL-1ß) as well as anti-inflammatory compounds, soluble TNF-Receptor p55 (sTNFRp55), sTNFRp75 and IL-1 receptor antagonist (sIL-1Ra), were investigated in 34 Brazilian cases of dengue fever (DF) originated from a study of exanthematic virosis. The presence of pro-inflammatory cytokines was detected in sera from these patients by ELISA. TNF-[alfa] and IL-6 levels were significantly higher than control subjects in 32 (por cento) and 52(por cento) patients, respectively. To our knowledge this was the first time a receptor antagonist and soluble receptors for cytokines were detected in sera obtained during exanthematic DF without hemorrhagic manifestations. Both sTNFRp55 and sTNFRp75 were consistently elevated in 42 (por cento) and 84 (por cento) patients, respectively. Most patients had IL-1ß levels not different from those of normal subjects, except for one case. Only 16 (por cento) patients had altered levels of IL-Ra. Previous studies in dengue hemorrhagic fever patients demonstrated production of these soluble factors; here we observed that they are found in absence of hemorrhagic manifestations. The possible role of these anti-inflammatory compounds in immune cell activation and in regulating cytokine-mediated pathogenesis during dengue infection is discussed.

Role of cytokines, prostaglandins and nitric oxide in hepatic regeneration

The liver is considered the center of the metabolism. Many of its functions are controlled by a network of mediators. Hepatic regeneration is a highly regulated event also by several substances. Herein is was reviewed the literature about the role of cytokines, prostaglandins and nitric oxide in this event. Prior, it was described the known activities of each substance in the body. Further, it was examined since the production until the action of each one in regenerating livers. We could conclude that some of these mediators present a well-defined action, while others are object of great controversy. Overall, the comprehension of the liver's regeneration is very important in concern to develop new kinds of treatment in hepatology.

Pielonefritis, mecanismos patogénicos

La presencia de bacterias a nivel de la mucosa de las vías urinarias determina una respuesta inflamatoria. El factor responsable de la invasión de células inflamatorias es la IL6 (interleuquina 6) y los componentes bacterianos inductores son las adhesinas y el LPS de la membrana bacteriana. La actividad inflamatoria no es sólo responsable de los síntomas agudos sino de la eliminación bacteriana. En los estudios experimentales, los animales no reactivos al LPS fueron incapaces de eliminar las bacterias y en embarazadas se ha demostrado que una respuesta menor de IL6 puede relacionarse con la mayor incidencia de pielonefritis (1-4). La respuesta inflamatoria también ha sido relacionada con la producción de IL8 (interleuquina 8). Estudios en humanos han mostrado correlación entre concentración de IL8 urinaria y los recuentos leucocitarios (5).

Expression of interleukin-6 in polymorphic reticulosis: immunohistochemical study of 5 cases

Peripheral T cell lymphoma encompasses lymphomas with a variety of histologic appearances and clinical patterns. Recently, it has been suggested that almost all of the histologic features described under the name of polymorphic reticulosis(PR), lethal midline granuloma, and midline malignant reticulosis can be included in those generally described for malignant lymphomas of peripheral T cell origin(PTCL). There have been few studies of pathogenesis or tissue damage mechanism in PR patients. The need for a precise mechanism for tissue damage has important therapeutic implications. Using immunohistochemical methods with polyclonal anti IL-6 antibody, the authors describe 5 cases of PR with clinically and pathologically typical PR demonstrating a high expression of IL-6. According to classification, 2 cases of grade 1 PR showed the highest expressions, and 2 cases of grade 2 PR with atypical lymphoid cells showed moderate activity, but one case progressed into frank lymphoma(grade 3) and lost IL-6 expression. This strongly implies that some cases of PR have a different mechanism of tissue damage from frank PTCL, despite the one disease spectrum. Further studies on more cases may help clarify the pathogenesis.