Fazli Demirturk, Hakan Aytan, Ahmet C Caliskan, Pelin Aytan, Dogan R Koseoglu
{"title":"过氧化物酶体增殖物激活受体激动剂罗格列酮对实验性大鼠子宫内膜异位症的诱导作用。","authors":"Fazli Demirturk, Hakan Aytan, Ahmet C Caliskan, Pelin Aytan, Dogan R Koseoglu","doi":"10.1016/j.jsgi.2005.10.002","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To assess the effect of the peroxisome proliferator-activated receptor (PPAR)-gamma agonist rosiglitazone on the induction of endometriosis in a rat model.</p><p><strong>Methods: </strong>Endometriosis was surgically induced in 28 rats by transplanting an autologous fragment of endometrial tissue onto the inner surface of the abdominal wall. Group I was assigned as control and no medication was administered. Starting 3 days before the operation and continuing for 4 weeks, 0.2 mg/kg/d rosiglitazone was administered to the study group orally. Four weeks later rats were killed and ectopic uterine tissues were evaluated morphologically and histologically. Scoring systems were used to evaluate preservation of epithelia.</p><p><strong>Results: </strong>Four rats in the study group and one rat in the control group died of complications related to surgery. There was a significant difference in post-treatment spherical volumes (64.00 mm3 [interquartile range (IQR): 354.42] vs 41.60 mm3 [IQR: 37.87], P = .018) and explant weights (77.97 mg [IQR: 431.27] vs 47.24 mg [IQR: 43.01], P = .005) between control and rosiglitazone-treated groups. The epithelia were found to be preserved significantly better in the control group when compared with the roziglitazone-treated group (2.00 [IQR:2.00] vs 0.00 [IQR:2.25], P = .014).</p><p><strong>Conclusions: </strong>Rosiglitazone was found to affect the induction of endometriosis negatively in this experimental rat model and seemed to interfere with the growth and maintenance of the uterine explant.</p>","PeriodicalId":17373,"journal":{"name":"Journal of the Society for Gynecologic Investigation","volume":"13 1","pages":"58-62"},"PeriodicalIF":0.0000,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.jsgi.2005.10.002","citationCount":"45","resultStr":"{\"title\":\"Effect of peroxisome proliferator-activated receptor-gamma agonist rosiglitazone on the induction of endometriosis in an experimental rat model.\",\"authors\":\"Fazli Demirturk, Hakan Aytan, Ahmet C Caliskan, Pelin Aytan, Dogan R Koseoglu\",\"doi\":\"10.1016/j.jsgi.2005.10.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To assess the effect of the peroxisome proliferator-activated receptor (PPAR)-gamma agonist rosiglitazone on the induction of endometriosis in a rat model.</p><p><strong>Methods: </strong>Endometriosis was surgically induced in 28 rats by transplanting an autologous fragment of endometrial tissue onto the inner surface of the abdominal wall. 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引用次数: 45
摘要
目的:探讨过氧化物酶体增殖物激活受体(PPAR)- γ激动剂罗格列酮对大鼠子宫内膜异位症的诱导作用。方法:将自体子宫内膜组织片段移植到腹壁内表面,手术诱导28只大鼠子宫内膜异位症。第一组为对照组,不给药。研究组从术前3 d开始,连续4周口服罗格列酮0.2 mg/kg/d。4周后处死大鼠,对异位子宫组织进行形态学和组织学观察。评分系统用于评估上皮的保存情况。结果:研究组4只大鼠,对照组1只大鼠死于手术并发症。对照组和罗格列酮处理组处理后球囊体积(64.00 mm3[四分位间距(IQR): 354.42] vs 41.60 mm3 [IQR: 37.87], P = 0.018)和外植体重量(77.97 mg [IQR: 431.27] vs 47.24 mg [IQR: 43.01], P = 0.005)差异有统计学意义。与罗格列酮治疗组相比,对照组的上皮保存情况明显更好(2.00 [IQR:2.00] vs 0.00 [IQR:2.25], P = 0.014)。结论:在本实验大鼠模型中发现罗格列酮对子宫内膜异位症的诱导有负向影响,并可能干扰子宫外植体的生长和维持。
Effect of peroxisome proliferator-activated receptor-gamma agonist rosiglitazone on the induction of endometriosis in an experimental rat model.
Objective: To assess the effect of the peroxisome proliferator-activated receptor (PPAR)-gamma agonist rosiglitazone on the induction of endometriosis in a rat model.
Methods: Endometriosis was surgically induced in 28 rats by transplanting an autologous fragment of endometrial tissue onto the inner surface of the abdominal wall. Group I was assigned as control and no medication was administered. Starting 3 days before the operation and continuing for 4 weeks, 0.2 mg/kg/d rosiglitazone was administered to the study group orally. Four weeks later rats were killed and ectopic uterine tissues were evaluated morphologically and histologically. Scoring systems were used to evaluate preservation of epithelia.
Results: Four rats in the study group and one rat in the control group died of complications related to surgery. There was a significant difference in post-treatment spherical volumes (64.00 mm3 [interquartile range (IQR): 354.42] vs 41.60 mm3 [IQR: 37.87], P = .018) and explant weights (77.97 mg [IQR: 431.27] vs 47.24 mg [IQR: 43.01], P = .005) between control and rosiglitazone-treated groups. The epithelia were found to be preserved significantly better in the control group when compared with the roziglitazone-treated group (2.00 [IQR:2.00] vs 0.00 [IQR:2.25], P = .014).
Conclusions: Rosiglitazone was found to affect the induction of endometriosis negatively in this experimental rat model and seemed to interfere with the growth and maintenance of the uterine explant.