15 research outputs found

    Immunoexpression of cyclooxygenase-1 and -2 in ulcerative colitis

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    Ulcerative colitis (UC) is a disease of the colon and rectum characterized by a nonspecific chronic inflammation mediated by the concerted response of cellular and humoral events. Prostaglandins are synthesized by cyclooxygenase (COX)-1 and -2 and exhibit both pro- and anti-inflammatory activity. To evaluate COX-1 and COX-2 immunoexpression in 42 cases of UC and to correlate it with clinicopathological parameters, COX-1 and COX-2 expression was investigated by the immunohistochemistry method. Only patients with all pertinent clinical and evolutive data as well as with adequate biopsy material were included in the study. Fifteen samples of colorectal adenocarcinoma and 14 of large bowel with no histological changes were used for positive and negative controls, respectively. UC patients showed COX-1 immunoreactivity in epithelial cells in 29% of the cases and in inflammatory cells in 43%. COX-2 positivity in epithelial and inflammatory cells was found in 69% of the samples. The comparison between UC and the control groups revealed that the UC group had significantly more positive cases for COX-1 and COX-2 in inflammatory cells. Immunohistochemistry allowed the identification of COX-1 and COX-2 expression in epithelial and inflammatory cells in UC biopsies. No significant difference between COX-1 and COX-2 immunoreactivity in epithelial and inflammatory cells was observed regarding the clinicopathological parameters. COX-2 presented low expression in normal colon and high expression in colorectal adenocarcinoma. COX-2 might play a role in the pathophysiologic processes of inflammatory bowel disease and the development of neoplasia. Treatment with selective COX-2 inhibitors might be an additional option for therapy

    Experimental study comparing meshes made of polypropylene, polypropylene plus polyglactin and polypropylene plus titanium: inflammatory cytokines, histological changes and morphometric analysis of collagen

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    Incisional hernia occurs in approximately 11% of all laparotomies. Changes in collagen have been closely implicated in its pathogenesis. the high recurrence rate (45-54%) after primary suture has stimulated the development of meshes. Currently, meshes are the biomaterials implant group most used in medicine. This study aims to compare the serum and tissue inflammatory responses and collagen deposition caused by meshes made of polypropylene, polypropylene + polyglactin and polypropylene + titanium.Thirty Wistar rats were divided into three groups. in group I, a high-density polypropylene mesh was positioned on the abdominal wall. in groups II and III, low-density meshes were used in associations with polyglactin and titanium, respectively. Immediately before the operation and on the first, third and fortieth postoperative days, pro-inflammatory cytokines were assayed. On the 40th postoperative day, the region of the inserted prosthesis was biopsied. the tissue inflammatory reaction was evaluated using a scale for objective scoring. for collagen, picrosirius was used with data reading using the Image Tool computer software.Cytokines: there were no statistically significant differences between the groups. Histology: on the 40th postoperative day in group I, there were fewer inflammatory tissue response and greater collagen deposition (P < 0.01). in group II, there were greater inflammatory tissue response and less collagen deposition (P < 0.01). Group III presented intermediate values between groups I and II.There were no significant differences in cytokine levels between the groups in the present study. in the animals with the polypropylene + polyglactin mesh implant there was the most intense inflammatory process with lower tissue maturation and collagen deposition on the 40th postoperative day. the polypropylene mesh presented a less severe late inflammatory process, with greater tissue maturation and collagen deposition. the polypropylene + titanium mesh presented intermediate values between the others.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Universidade Federal de São Paulo, BR-04024002 São Paulo, BrazilUniversidade Federal de São Paulo, BR-04024002 São Paulo, BrazilFAPESP: 07/57100-6Web of Scienc
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