Effect of Fugongning on morphology and protein expression of caspase-3 and Bcl-2 in rat endometriotic cells

AIM:To investigate the effect of Fugongning(FGN) on treating endometriosis(EMT) by observing the changes of histopathological morphology and ultrastructure,and the expression of caspase-3 and Bcl-2 in an endometriotic rat model.METHODS:The rat model of EMT was established by autotransplantation of endometrium,and the model rats were randomly divided into 4 groups:EMT group,danazol group,FGN 1 group and FGN 2 group.The rats were treated with normal saline in EMT group,danazol in danazol group and different doses of FGN in FGN 1 group and FGN 2 group by intragastric administration for 4 weeks.After 4 weeks of treatment,the size of the lesion and histopathological morphology of ectopic endometrial tissues were observed under transmission electron microscope.Using immunohistochemistry method,the protein expression of caspase-3 and Bcl-2 in endometrium and endometriotic tissues was determined.RESULTS:The size of transplanted object in FGN treatment groups was much smaller than that in control group,and the growth of focus was inhibited.Under the electron microscope,the ectopic endometrial tissues in FGN treatment groups and damazol group shrinked,glandular epithelium became thinner,and the number of the glands decreased.Ectopic endome-trial cells were shot-cylindrical even tabular with incompact arrangement,and apoptosis and interstitial fibrosis were observed.Eutopic endometria didn't show any pathological changes.Besides,mitochondrion swelling and low,disappeared or vacuolated mitochondrial crista in ectopic endometrial cells were observed.Immunohistochemistry results showed that higher expression of Bcl-2 protein in ectopic endometrial tissue in EMT group was observed.The protein level of caspase-3 in the ectopic endometrial cells in FGN treatment groups increased,while the protein expression of Bcl-2 decreased,thus promoting the apoptosis of the ectopic endometrial cells.CONCLUSION:FGN inhibits the proliferation of ectopic endometrium by inducing the apoptosis of endometriotic cells through activating caspase activity and reducing Bcl-2 expression in the cells.