Amygdalin inhibits endometrial stromal cell proliferation, migration, and invasion in endometriosis mice via inhibiting Wnt/β-catenin signaling.

Abstract

To explore the impact of amygdalin on the proliferation, migration, and invasion of human endometrial stromal cells (HESCs) and the possible underlying mechanism. HESCs were incubated with 50, 100, and 200&#xa0;&#xb5;g/mL of amygdalin. The malignant activities of HESCs were analyzed by functional experiments. The activation of the Wnt/&#x3b2;-catenin signaling was tested using TOP/FOPFlash. The mRNA expressions of genes were validated by qRT-PCR. The endometriosis (EMS) mouse model was induced and the impact of amygdalin on the growth of ectopic endometrial lesions were assessed. It was observed that amygdalin markedly lessened the malignant activities of HESCs in a dose-dependent way (p&#x2009;<&#x2009;0.05). Amygdalin dose-dependently declined the activation of TOPFlash and mRNA levels of &#x3b2;-catenin, cyclinD1 and c-Myc in HESCs (p&#x2009;<&#x2009;0.05). Additionally, the increasing dose of amygdalin progressively inhibited the growth of ectopic endometrial lesions in EMS mouse model (p&#x2009;<&#x2009;0.05). We reached a conclusion that amygdalin could inhibit the malignant activities of HESCs and alleviate EMS, which was related to Wnt/&#x3b2;-catenin signaling activation.