Effect of pentoxifylline on vascular endothelial growth factor C and flk-1 expression on endometrial implants in the rat endometriosis model
Objective To investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis model. Design Prospective, randomized, placebo-controlled study. Setting Academic institution. Animal(s) Twenty Wistar rats with surgically induced end...
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| Published in | Fertility and sterility Vol. 93; no. 4; pp. 1316 - 1323 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
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Elsevier Inc
01.03.2010
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| Abstract | Objective To investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis model. Design Prospective, randomized, placebo-controlled study. Setting Academic institution. Animal(s) Twenty Wistar rats with surgically induced endometriosis. Intervention(s) Animals were evaluated after surgical induction of endometriosis and random allocation to a group that received pentoxifylline and a control group that received NaCl 0.9%, for 3 weeks. At the end of the treatment period the animals were killed and the implants evaluated macroscopically as well as by immunohistochemistry. Main Outcome Measure(s) Morphologic changes of the endometriotic implants; and evaluation of VEGF-C and flk-1 expression by a semiquantitative analysis (HSCORE) for the intensity of immunohistochemical reactivity. Result(s) A significant reduction was observed in the mean volume of the endometriotic implants per animal in the treatment group as compared with the control group. There was a significant reduction not only in the mean volume of implants per animal but also in the mean number of implants per animal after treatment. By immunohistochemical evaluation (HSCORE), there was a significant reduction in VEGF-C expression after treatment in all areas examined. A significant reduction of flk-1 expression was also noted in the glandular compartment after treatment but not in the epithelial surface or stroma. Conclusion(s) Pentoxifylline may cause suppression of endometriotic lesions by suppressing angiogenesis through VEGF-C and flk-1 expression. |
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| AbstractList | Objective To investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis model. Design Prospective, randomized, placebo-controlled study. Setting Academic institution. Animal(s) Twenty Wistar rats with surgically induced endometriosis. Intervention(s) Animals were evaluated after surgical induction of endometriosis and random allocation to a group that received pentoxifylline and a control group that received NaCl 0.9%, for 3 weeks. At the end of the treatment period the animals were killed and the implants evaluated macroscopically as well as by immunohistochemistry. Main Outcome Measure(s) Morphologic changes of the endometriotic implants; and evaluation of VEGF-C and flk-1 expression by a semiquantitative analysis (HSCORE) for the intensity of immunohistochemical reactivity. Result(s) A significant reduction was observed in the mean volume of the endometriotic implants per animal in the treatment group as compared with the control group. There was a significant reduction not only in the mean volume of implants per animal but also in the mean number of implants per animal after treatment. By immunohistochemical evaluation (HSCORE), there was a significant reduction in VEGF-C expression after treatment in all areas examined. A significant reduction of flk-1 expression was also noted in the glandular compartment after treatment but not in the epithelial surface or stroma. Conclusion(s) Pentoxifylline may cause suppression of endometriotic lesions by suppressing angiogenesis through VEGF-C and flk-1 expression. OBJECTIVETo investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis model.DESIGNProspective, randomized, placebo-controlled study.SETTINGAcademic institution.ANIMAL(S)Twenty Wistar rats with surgically induced endometriosis.INTERVENTION(S)Animals were evaluated after surgical induction of endometriosis and random allocation to a group that received pentoxifylline and a control group that received NaCl 0.9%, for 3 weeks. At the end of the treatment period the animals were killed and the implants evaluated macroscopically as well as by immunohistochemistry.MAIN OUTCOME MEASURE(S)Morphologic changes of the endometriotic implants; and evaluation of VEGF-C and flk-1 expression by a semiquantitative analysis (HSCORE) for the intensity of immunohistochemical reactivity.RESULT(S)A significant reduction was observed in the mean volume of the endometriotic implants per animal in the treatment group as compared with the control group. There was a significant reduction not only in the mean volume of implants per animal but also in the mean number of implants per animal after treatment. By immunohistochemical evaluation (HSCORE), there was a significant reduction in VEGF-C expression after treatment in all areas examined. A significant reduction of flk-1 expression was also noted in the glandular compartment after treatment but not in the epithelial surface or stroma.CONCLUSION(S)Pentoxifylline may cause suppression of endometriotic lesions by suppressing angiogenesis through VEGF-C and flk-1 expression. To investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis model. Prospective, randomized, placebo-controlled study. Academic institution. Twenty Wistar rats with surgically induced endometriosis. Animals were evaluated after surgical induction of endometriosis and random allocation to a group that received pentoxifylline and a control group that received NaCl 0.9%, for 3 weeks. At the end of the treatment period the animals were killed and the implants evaluated macroscopically as well as by immunohistochemistry. Morphologic changes of the endometriotic implants; and evaluation of VEGF-C and flk-1 expression by a semiquantitative analysis (HSCORE) for the intensity of immunohistochemical reactivity. A significant reduction was observed in the mean volume of the endometriotic implants per animal in the treatment group as compared with the control group. There was a significant reduction not only in the mean volume of implants per animal but also in the mean number of implants per animal after treatment. By immunohistochemical evaluation (HSCORE), there was a significant reduction in VEGF-C expression after treatment in all areas examined. A significant reduction of flk-1 expression was also noted in the glandular compartment after treatment but not in the epithelial surface or stroma. Pentoxifylline may cause suppression of endometriotic lesions by suppressing angiogenesis through VEGF-C and flk-1 expression. |
| Author | Lai, Joseph, M.D Gregoriou, Odysseas, M.D Deliveliotou, Aikaterini, M.D Vlahos, Nikos F., M.D Vlachos, Athanasios, M.D Creatsas, George, M.D Perrea, Despoina, Ph.D Zhao, Yulian, Ph.D |
| Author_xml | – sequence: 1 fullname: Vlahos, Nikos F., M.D – sequence: 2 fullname: Gregoriou, Odysseas, M.D – sequence: 3 fullname: Deliveliotou, Aikaterini, M.D – sequence: 4 fullname: Perrea, Despoina, Ph.D – sequence: 5 fullname: Vlachos, Athanasios, M.D – sequence: 6 fullname: Zhao, Yulian, Ph.D – sequence: 7 fullname: Lai, Joseph, M.D – sequence: 8 fullname: Creatsas, George, M.D |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19147132$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1111_jog_12434 crossref_primary_10_1093_humupd_dms026 crossref_primary_10_1016_j_bpobgyn_2019_06_006 crossref_primary_10_1016_j_fertnstert_2016_12_025 crossref_primary_10_1038_s41598_024_57850_0 crossref_primary_10_1253_circj_CJ_09_0135 crossref_primary_10_1097_RD9_0000000000000053 crossref_primary_10_3109_09513590_2011_593669 crossref_primary_10_23736_S2724_606X_21_04776_X crossref_primary_10_4236_arsci_2016_42008 crossref_primary_10_1016_j_fertnstert_2012_07_1120 crossref_primary_10_3892_mmr_2018_9744 crossref_primary_10_3389_fgwh_2022_856316 crossref_primary_10_1155_2014_191967 crossref_primary_10_2217_whe_15_51 crossref_primary_10_1016_j_autrev_2018_03_017 crossref_primary_10_1002_med_21802 crossref_primary_10_1002_14651858_CD007677_pub4 crossref_primary_10_1080_08941939_2017_1317374 crossref_primary_10_1097_OGX_0000000000000888 crossref_primary_10_1177_1933719116673198 crossref_primary_10_3390_cells12081199 crossref_primary_10_1016_j_ejphar_2018_03_015 crossref_primary_10_7717_peerj_5434 |
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| Copyright | American Society for Reproductive Medicine 2010 American Society for Reproductive Medicine Copyright 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved. |
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| Keywords | Endometriosis pentoxifylline flk-1 rat angiogenesis VEGF |
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| Snippet | Objective To investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis model.... To investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis model. Prospective,... OBJECTIVETo investigate the effects of pentoxifylline, on vascular endothelial growth factor (VEGF)-C and flk-1 expression in the rat endometriosis... |
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| SubjectTerms | angiogenesis Angiogenesis Inhibitors - pharmacology Animals Disease Models, Animal Endometriosis Endometriosis - drug therapy Endometriosis - metabolism Endometriosis - surgery Endometrium - drug effects Endometrium - metabolism Endometrium - transplantation Female flk-1 Infertility, Female - drug therapy Infertility, Female - metabolism Infertility, Female - surgery Internal Medicine Obstetrics and Gynecology pentoxifylline Pentoxifylline - pharmacology Prospective Studies Random Allocation rat Rats Rats, Wistar Transplants Vascular Endothelial Growth Factor C - biosynthesis Vascular Endothelial Growth Factor Receptor-2 - biosynthesis VEGF |
| Title | Effect of pentoxifylline on vascular endothelial growth factor C and flk-1 expression on endometrial implants in the rat endometriosis model |
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