Introduction: Endometriosis is a medical condition in which there is abnormal growth of tissue resembling the endometrium outside the uterus. It can cause symptoms of pain and/or infertility. The current medical therapy focuses on reducing estradiol levels or stimulating progesterone response. One of the most effective options for medical treatment is the use of GnRH analogs. Dienogest have a direct anti-inflammatory effect on endometriotic stromal cells. However, a comparison of the anti-inflammatory effects of these drugs on IFN-Ɣ has not been previously investigated. Therefore, this study aims to compare the effects of reducing IFN-Ɣ by both Dienogest and Leuprolide Acetat in a mouse model. Material and Methods: This study employed a post-test only control group design and involved 4 groups, namely the negative control group, positive control group, and two treatment groups: one group administered Dienogest at a dosage of 0.0052 milligrams per day for 14 days, and the other administered Leuprolide Acetat at a dosage of 0.00975 milligrams once every 5 days for a period of 14 days. Serum IFN-Ɣ levels were measured using Enzyme-Linked Immunosorbent Assay (ELISA). The data were subsequently analyzed using IBM SPSS 25 with One-Way ANOVA test. Results: This study demonstrated that Leuprolide Acetat significantly decreased serum levels of IFN-Ɣ, whereas Dienogest actually increased the levels . Conclusion: In a mouse model of endometriosis (Mus musculus), Leuprolide Acetat effectively reduced the levels of IFN-Ɣ (pro-inflammatory). Conversely, Dienogest increased the levels of IFN-Ɣ (anti-inflammatory) in the mouse model of endometriosis.
CITATION STYLE
Maria Antonia Barbara Batu Mali, Siskanita Nur Fitriana, Sutrisno, S., Husnul Khotimah, I Wayan Arsana Wiyasa, I Wayan Agung Indrawan, & Maharani, M. (2023). Comparison of the Effects of Dienogest and Leuprolide Acetat on Serum Interferon (IFN-Ɣ) Levels in a Mouse Model of Endometriosis (Mus musculus). Asian Journal of Health Research, 2(2), 3–9. https://doi.org/10.55561/ajhr.v2i2.111
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