The effect of calcineurin signaling inhibition on the treatment of endometriosis in rats

Abstract Objective The molecular and cellular mechanism underlying endometriosis is still under investigation. CypA is one of the inflammatory marker which secreted various type of cell in the inflammatory condition. During the inflammation, CypA exacerbate inflammatory response by the activation of calcineurin signaling that increases the cytokine secretion and tissue degradation in inflammatory region. The aim of this study was to investigate the effect of calcineurin signaling inhibition on the treatment endometriosis in rats. Materials & Methods In the present study, 32 albino-wistar rat were used. All rats were divided into three groups as Cyclosporin A (n = 10), tacrolimus (n = 10) and control group (n = 12). Cyclosporin A group was administered intraperitoneal and tacrolimus group was administered intravenous, total 2 doses at intervals of 2 weeks respectively. All studies lasted for 8 weeks. Processed endometrial tissues will cut at the middle of the tissue samples and embedded into paraffin. Histological sections (5 µm) were stained with Ki-67, Bcl-2, Caspase-3 and VEGF. Results The size of endometriotic focus were 204.7 ± 153.4 mm3, 71.9 ± 85.4 mm3 ve 30.6 ± 36.7 mm3 in control, in CsA and in tacrolimus groups. Compared the control group the size of endometriotic focus was lower in CsA and tacrolimus group (p = 0.002). Microscopically, Ki-67 (p = 0.010) and VEGF (p = 0.007) immunoreactivity were lower in CsA and tacrolimus group than controls. Conclusion The inhibition of calcineurin signaling with CsA and tacrolimus treatment causes regression of endometriotic focus via decreases of endometriotic cell proliferation and angiogenesis in ectopic endometriotic tissue.