内异方对子宫内膜异位症大鼠异位子宫内膜细胞凋亡的影响OA

Objective To investigate the effects and possible mechanisms of Neiyi Prescription(NYP)on ectopic endometrial tissue apoptosis.Methods Twenty-four female SD rats were randomly assigned to a control group(2 ml/d of normal saline,n=6),a model group(2 ml/d of normal saline,n=6),a low-dose NYP group(0.63 g/kg,n=6),and a high-dose NYP group(1.26 g/kg,n=6).Except for the control group,the other groups received autologous transplantation to construct an endometriosis(EMs)rat model.Gavage was performed on every group twice a day for 3 consecutive weeks.Afterwards,the following parameters were determined by different methods:the inhibitory rate on ectopic endometrial cysts by NYP calculated using formula,tissue morphology by the hematoxylin-eosin(HE)staining,apoptosis rate by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)staining,and Protein Kinase B(AKT1)expression by the immunohistochemical(IHC)staining.Results Compared with the control group,the model group exhibited tightly packed epithelial cells in an irregular manner,increased interstitial cells,decreased apoptosis rate(P<0.001),and increased AKT1 positivity(P<0.001).After intervention with normal saline,the model group exhibited increased cyst volume,while the low-and high-dose NYP groups exhibited decreased cyst volume to varying degrees.Compared to the model group,a significant inhibitory rate on ectopic endometrial cysts was observed in both low-and high-dose NYP groups(P<0.05).In the low-dose NYP group,the epithelial cells were more regularly arranged,with a decreased number of interstitial cells.In both low-and high-dose NYP groups,a dose-dependent increase was observed in apoptosis rate(P<0.001).The AKT1 positivity rate was reduced in the NYP groups(P<0.01).Compared to the low-dose NYP group,the high-dose NYP group exhibited looser epithelial cell arrangement and decreased interstitial cells in a more uniform distribution.Conclusion High-dose NYP may exert therapeutic effects by down-regulating AKT1 expression,thereby promoting apoptosis and inhibiting ectopic endometrial cyst growth in EMs rats.