Effects of cisplatin on surgically induced endometriosis in a rat model.
Oncol Lett
; 16(4): 5282-5290, 2018 Oct.
Article
em En
| MEDLINE
| ID: mdl-30250597
Research has strongly suggested that the features of endometriosis serve as a precursor lesion of ovarian cancer. Cisplatin (CDDP) is the preferred drug against these cancer types. The present study investigated the effects of CDDP on surgically induced endometriosis in a rat model. Endometriosis was surgically induced by the autologous transplantation of endometrial tissue. A total of 36 model rats were randomly divided into three groups. The rats in Group 1 (control group, n=12) received no medication. The rats in Group 2 (n=12) and Group 3 (n=12) were administered 35 mg/m2 CDDP and 70 mg/m2 CDDP, respectively, every four days. All rats were treated for a total of 24 days. The growth and histologic scores of the implants were calculated. The expression of protein markers, including vascular endothelial growth factor (VEGF), aromatase P450 (P450arom), transforming growth factor-ß (TGF-ß) and matrix metalloproteinase (MMP)-2, were assessed using immunohistochemistry, an enzyme-linked immunosorbent assay and western blot analysis. Following CDDP treatment, the mean implant sizes were significantly reduced in Groups 2 and 3 compared with the control group (P=0.01). The mean histologic scores were also significantly lower in Groups 2 and 3. Furthermore, the protein expression of VEGF, P450arom, TGF-ß and MMP-2 was significantly lower in Groups 2 and 3 when compared with the control group. A loss of hair was observed in 4 rats, which only occurred in Group 3. A dose-dependent effect was observed in the two CDDP-treated groups. In conclusion, the expression of proliferation- and angiogenesis-associated proteins was significantly lower following treatment with CDDP. CDDP caused a significant regression in the size of the endometriotic implants and induced atrophy of these lesions in rats.
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MEDLINE
Tipo de estudo:
Prognostic_studies
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article