Effect of caffeic acid phenethyl ester on the regression of endometrial explants in an experimental rat model

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Caffeic acid phenethyl ester treatment reduced endometrial explant volume, weight, and COX-2 expression, while decreasing peritoneal MDA levels and increasing SOD and CAT activities in a rat endometriosis model.

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This study evaluated whether caffeic acid phenethyl ester (CAPE), an antioxidant/anti-inflammatory agent, could induce regression of experimentally induced endometriosis in 30 rats over 4 weeks, comparing intraperitoneal CAPE (10 µmol/kg/day) versus vehicle. Researchers assessed implant volume and weight changes, performed histologic and immunohistochemical analyses of endometriotic explants (including COX-2 positivity in glandular epithelium), and measured peritoneal superoxide dismutase (SOD) and catalase (CAT) activities and malondialdehyde (MDA) levels as oxidative stress markers. CAPE treatment produced significantly smaller, lighter explants, lower COX-2 positivity scores, histologic evidence of atrophy/regression, and significantly decreased peritoneal MDA with reduced SOD/CAT activity versus controls (P < .01). A key limitation is that the experiment used an animal model with intraperitoneal dosing and relatively small group sizes, which may not directly translate to human disease. This paper is centrally about endometriosis — it tests CAPE’s ability to regress experimental endometrial explants in a rat model while examining oxidative stress and COX-2-related changes.

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Abstract

The objective of this study is to determine the effects of antioxidant and anti-inflammatory caffeic acid phenethyl ester (CAPE) on experimental endometriosis, peritoneal superoxide dismutase (SOD) and catalase (CAT) activities, and malondialdehyde (MDA) levels in the rat endometriosis model. Thirty rats with experimentally induced endometriosis were randomly divided into 2 groups and treated for 4 weeks with intraperitoneal CAPE (CAPE-treated group; 10 micromol/kg/d, n = 13) or vehicle (control group; n = 13). The volume and weight changes of the implants were calculated. Immunohistochemical and histologic examinations of endometriotic explants by semiquantitative analysis and measurements of peritoneal SOD, CAT, and MDA levels were made. Following 4 weeks of treatment with CAPE, there were significant differences in posttreatment spherical volumes (37.4 +/- 14.7 mm(3) vs 147.5 +/- 41.2 mm(3)) and explant weights (49.1 +/- 28.5 mg vs 158.9 +/- 50.3 mg) between the CAPE-treated groups and controls. The mean evaluation nomogram levels in glandular epithelium for COX-2 positivity by scoring system were 2.1 +/- 0.3 in the CAPE-treated group and 3.9 +/- 0.3 in the control group. In the CAPE-treated group, peritoneal levels of MDA and activities of SOD and CAT significantly decreased when compared with the control group (P < .01). Histologic analysis of the explants demonstrated mostly atrophy and regression in the treatment group, and semiquantitative analysis showed significantly lower scores in rats treated with CAPE compared with the control group. CAPE appeared to cause regression of experimental endometriosis.
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Abstract

The objective of this study is to determine the effects of antioxidant and anti-inflammatory caffeic acid phenethyl ester (CAPE) on experimental endometriosis, peritoneal superoxide dismutase (SOD) and catalase (CAT) activities, and malondialdehyde (MDA) levels in the rat endometriosis model. Thirty rats with experimentally induced endometriosis were randomly divided into 2 groups and treated for 4 weeks with intraperitoneal CAPE (CAPE-treated group; 10 µ mol/kg/d, n = 13) or vehicle (control group; n = 13). The volume and weight changes of the implants were calculated. Immunohistochemical and histologic examinations of endometriotic explants by semiquantitative analysis and measurements of peritoneal SOD, CAT, and MDA levels were made. Following 4 weeks of treatment with CAPE, there were significant differences in posttreatment spherical volumes (37.4 ± 14.7 mm 3 vs 147.5 ± 41.2 mm 3) and explant weights (49.1 ± 28.5 mg vs 158.9 ± 50.3 mg) between the CAPE-treated groups and controls. The mean evaluation nomogram levels in glandular epithelium for COX-2 positivity by scoring system were 2.1 ± 0.3 in the CAPE-treated group and 3.9 ± 0.3 in the control group. In the CAPE-treated group, peritoneal levels of MDA and activities of SOD and CAT significantly decreased when compared with the control group (P <.01). Histologic analysis of the explants demonstrated mostly atrophy and regression in the treatment group, and semiquantitative analysis showed significantly lower scores in rats treated with CAPE compared with the control group. CAPE appeared to cause regression of experimental endometriosis. Similar content being viewed by others

References

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endometriosis

MeSH descriptors

Antioxidants Caffeic Acids Endometriosis Endometrium Phenylethyl Alcohol Animals Anti-Inflammatory Agents, Non-Steroidal Anti-Inflammatory Agents, Non-Steroidal Anti-Inflammatory Agents, Non-Steroidal Antioxidants Caffeic Acids Caffeic Acids Catalase Catalase Cyclooxygenase 2 Cyclooxygenase 2 Disease Models, Animal Endometriosis Endometriosis Endometriosis

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