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• W2015328173 abstract "ObjectiveMice that are deficient in PPAR-a exhibit a prolonged response to inflammatory stimuli, suggesting a modulatory effect of PPAR-α on inflammation. Numerous studies evaluated the effect of anti-inflammatory agents on endometriosis. We aimed to assess the effect of fenofibrate –a PPAR-α agonist- in a rat endometriosis model with prospective randomized study.DesignProspective randomized study.Materials and methodsEndometriosis was surgically induced in 40 rats by transplanting an autologous fragment of endometrial tissue onto the inner surface of the abdominal wall. After allowing 3 weeks for tissue growth, repeat laparotomies were performed on the animals to check the implants. After then animals were randomized into 4 groups; Group I: (controls) no medication; Group II: leuprolide acetate 1 mg/kg single dose, sc; Group III: low-dose fenofibrate (10 mg/kg/d, p.o.) and, Group IV: high-dose fenofibrate (100 mg/kg/d, p.o.). The treatment was initiated on the day of surgery and continuing for 3 weeks, was administered to the study groups. Three weeks later rats were killed and implants were evaluated morphologically. The immunohistochemical examination of the implants is underway at the time of writing of this abstract.ResultsAll rats, except 2 in group II survived throughout the study. All rats developed similar areas of implants at the second laparotomy. The treatment with leuprolide acetate, high dose or low dose fenofibrate caused significant decreases in the implant areas compared to the controls (P=0.03, P=0.003 and P=0.01, respectively). The mean areas of implants decreased from 20.2. ± 12.1 to 10.2 ± 5.9 mm2 after Leuprolide administration in Group II (P=0.008), from 33.1 ± 18.7 to 9.7 ± 9.2 mm2 in Group III (P=0.005), 35.8 ± 18.9 mm2 to17.9 ± 16.2 mm2 (P=0.007) whereas in Group I, the mean area did not change significantly (34.0 ± 13.8 vs. 33.3 ± 20.4 mm2; P=0.915).ConclusionsFenofibrate caused regression of endometriosis in this experimental rat model . The findings of this study provide a basis for further studies aimed at assessing fenofibrate as potential therapeutic agents in the treatment of endometriosis. ObjectiveMice that are deficient in PPAR-a exhibit a prolonged response to inflammatory stimuli, suggesting a modulatory effect of PPAR-α on inflammation. Numerous studies evaluated the effect of anti-inflammatory agents on endometriosis. We aimed to assess the effect of fenofibrate –a PPAR-α agonist- in a rat endometriosis model with prospective randomized study. Mice that are deficient in PPAR-a exhibit a prolonged response to inflammatory stimuli, suggesting a modulatory effect of PPAR-α on inflammation. Numerous studies evaluated the effect of anti-inflammatory agents on endometriosis. We aimed to assess the effect of fenofibrate –a PPAR-α agonist- in a rat endometriosis model with prospective randomized study. DesignProspective randomized study. Prospective randomized study. Materials and methodsEndometriosis was surgically induced in 40 rats by transplanting an autologous fragment of endometrial tissue onto the inner surface of the abdominal wall. After allowing 3 weeks for tissue growth, repeat laparotomies were performed on the animals to check the implants. After then animals were randomized into 4 groups; Group I: (controls) no medication; Group II: leuprolide acetate 1 mg/kg single dose, sc; Group III: low-dose fenofibrate (10 mg/kg/d, p.o.) and, Group IV: high-dose fenofibrate (100 mg/kg/d, p.o.). The treatment was initiated on the day of surgery and continuing for 3 weeks, was administered to the study groups. Three weeks later rats were killed and implants were evaluated morphologically. The immunohistochemical examination of the implants is underway at the time of writing of this abstract. Endometriosis was surgically induced in 40 rats by transplanting an autologous fragment of endometrial tissue onto the inner surface of the abdominal wall. After allowing 3 weeks for tissue growth, repeat laparotomies were performed on the animals to check the implants. After then animals were randomized into 4 groups; Group I: (controls) no medication; Group II: leuprolide acetate 1 mg/kg single dose, sc; Group III: low-dose fenofibrate (10 mg/kg/d, p.o.) and, Group IV: high-dose fenofibrate (100 mg/kg/d, p.o.). The treatment was initiated on the day of surgery and continuing for 3 weeks, was administered to the study groups. Three weeks later rats were killed and implants were evaluated morphologically. The immunohistochemical examination of the implants is underway at the time of writing of this abstract. ResultsAll rats, except 2 in group II survived throughout the study. All rats developed similar areas of implants at the second laparotomy. The treatment with leuprolide acetate, high dose or low dose fenofibrate caused significant decreases in the implant areas compared to the controls (P=0.03, P=0.003 and P=0.01, respectively). The mean areas of implants decreased from 20.2. ± 12.1 to 10.2 ± 5.9 mm2 after Leuprolide administration in Group II (P=0.008), from 33.1 ± 18.7 to 9.7 ± 9.2 mm2 in Group III (P=0.005), 35.8 ± 18.9 mm2 to17.9 ± 16.2 mm2 (P=0.007) whereas in Group I, the mean area did not change significantly (34.0 ± 13.8 vs. 33.3 ± 20.4 mm2; P=0.915). All rats, except 2 in group II survived throughout the study. All rats developed similar areas of implants at the second laparotomy. The treatment with leuprolide acetate, high dose or low dose fenofibrate caused significant decreases in the implant areas compared to the controls (P=0.03, P=0.003 and P=0.01, respectively). The mean areas of implants decreased from 20.2. ± 12.1 to 10.2 ± 5.9 mm2 after Leuprolide administration in Group II (P=0.008), from 33.1 ± 18.7 to 9.7 ± 9.2 mm2 in Group III (P=0.005), 35.8 ± 18.9 mm2 to17.9 ± 16.2 mm2 (P=0.007) whereas in Group I, the mean area did not change significantly (34.0 ± 13.8 vs. 33.3 ± 20.4 mm2; P=0.915). ConclusionsFenofibrate caused regression of endometriosis in this experimental rat model . The findings of this study provide a basis for further studies aimed at assessing fenofibrate as potential therapeutic agents in the treatment of endometriosis. Fenofibrate caused regression of endometriosis in this experimental rat model . The findings of this study provide a basis for further studies aimed at assessing fenofibrate as potential therapeutic agents in the treatment of endometriosis." @default.
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• W2015328173 title "Effect of peroxisome proliferator – activated receptor-α (PPAR-α) agonist-fenofibrate on the induction of endometriosis in an experimental rat model" @default.
• W2015328173 doi "https://doi.org/10.1016/j.fertnstert.2007.07.708" @default.
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