Proteomics analysis of the effects of erxian decoction on retarding ovarian aging

Abstract

BACKGROUND: Erxian decoction (EXD), a Chinese medicine formula, is widely used for relieving menopausal syndrome by preventing estrogen deficiency which is caused by ovarian aging, especially decrease in both the quantity and the quality of follicles. However, the in deepth action mechanism of the EXD on delaying ovarian aging has not been fully understood. OBJECTIVE: The present study was designed to investigate the effects of EXD on intervention of ovarian aging by comparing the changes in ovarian proteome profiles in Sprague-Dawley rats which were aged 3 months and 12 months without EXD treatment, as well as 12 months with EXD treatment. METHODOLOGY: 12-month-old SD rats (n=3) were treated with 4.1 mg/kg (EXD/rat) by oral administration for 2 weeks and 3-,12-month-old SD rats were treated with an equal volume of sterilized PBS by oral administration for 2 weeks as control (n=3 for each group). Ovarian proteome profiles were obtained by employing 2-dimensional electrophoresis and analyzed with PDQuest 2-DE Analysis Software. Protein spots of different expression levels were identified with tandem time-of-flight MS/MS system. The bioinformatics analysis was performed with Blast2GO software to obtain the assignment of protein functional terms. RESULTS: Proteomics analysis showed that the expression of 11 proteins, which were involved in cAMP-mediated signaling, metabolism, stress and anti-oxidation pathways, was >1.5 folds different after treating with EXD. Table 1 summarizes the classification, function and the level of expression (up-regulation or down-regulation) of the proteins. CONCLUSION: The results obtained from this study suggested that EXD prevents ovarian aging via the following pathway: (1) up-regulation of the steroidogenesis by activating cAMP-mediated signaling and down-regulation of progesterone catabolism (2) up-regulation of the antioxidant capacity (3) down regulation of extrinsic apoptotic signaling pathway, and (4) down-regulation of ATP metabolism which is a major source of oxidative stress.