Abstract
The aim of the present study was to evaluate the protective effects of combined atorvastatin and amygdalin in a rat model of endometriosis. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), matrix metalloproteinase-2 (MMP-2) and MMP-9 levels in the peritoneal fluid were determined. The expression of TNF-α, IL-6, MMP-2, and MMP-9 mRNA, and the levels of lipid peroxidation, reduced glutathione (GSH), superoxide dismutase (SOD), catalase, and glutathione peroxidase (Gpx) were measured. Histopathological analysis was also conducted. The results showed that peritoneal TNF-α, IL-6, MMP-2, and MMP-9 levels were reduced by > 50%, and mRNA expression was decreased. Lipid peroxidation was considerably reduced, while GSH, SOD, Gpx, and catalase levels increased by > 40%. Reductions in leukocyte infiltration and fibrosis following treatment were also observed. Thus, our study suggested that combined treatment consisting of atorvastatin and amygdalin attenuates endometriosis. A detailed investigation of molecular mechanism of atorvastatin and amygdalin in endometriosis is needed.
Highlights
Endometriosis is a gynecological disease of the endometrium, in which the endometrial tissue of the uterine lining grows outside the uterus, most commonly on the Fallopian tubes, ovaries and tissues around the ovaries and uterus (Sharpe-Timms 2002)
Simsek et al (2012) showed that amygdalin modulates the activities of local immune cells. Since these cells are an essential component of endometrial growth and development in endometriosis (Simsek et al 2012), in this study, we examined the potential protective effects of atorvastatin and amygdalin in Sprague-Dawley rats with experimentally induced endometriosis
The four groups used in this study were as follows: group I, sham-operated control; group II, untreated endometriosis; group III, endometriosis treated with atorvastatin (5 mg/kg) with amygdalin (5 mg/kg); and group IV, endometriosis treated with atorvastatin (10 mg/kg) with amygdalin (10 mg/kg)
Summary
Endometriosis is a gynecological disease of the endometrium, in which the endometrial tissue of the uterine lining grows outside the uterus (do Amaral et al 2009), most commonly on the Fallopian tubes, ovaries and tissues around the ovaries and uterus (Sharpe-Timms 2002). Infertility and pelvic pain are the primary symptoms of endometriosis (Bulletti et al 2010). Bulun (2009) reported that one in every seven women suffers from endometriosis, which causes infertility in 30–50% of cases. The lesions in endometriosis require cell adhesion, migration, and proliferation for development (Van. Langendonckt et al 2002; Giudice and Kao 2004). The treatment of endometriosis includes hormone therapy, such as androgen and gonadotropin-releasing hormone, and the use of non-steroidal anti-inflammatory drugs for pain relief (Garai et al 2006). Hormone therapy can result in side effects such as hot flushes and genital atrophy; there is a high rate of endometriosis recurrence (Garai et al 2006). A novel therapeutic drug for satisfactory treatment of endometriosis is needed
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