OBJECTIVE

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To investigate the improvement effects of Jinkui shenqi pills on polycystic ovary syndrome （PCOS） model rats and the mechanism.

METHODS

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Totally 40 rats were given letrozole suspension instragastrically （1 mg/kg， once a day， for consecutive 21 d） to induce PCOS model. Model rats were divided into model group， ethinylestradiol and cyproterone acetate tablets （short for diane-35）+metformin group （diane-35 0.2 mg/kg + metformin 230 mg/kg， as positive control）， Jinkui shenqi pills low-dose， medium-dose and high-dose groups （0.5， 1.0， 2.0 g/kg）， with 10 rats in each group. Other 10 healthy rats were included in normal group. Each group was given the corresponding drugs， once a day， for consecutive 30 d. Twelve hours after the last administration， serum levels of blood glucose， insulin， estrogen （E

2

）， testosterone （T）， gonadotropin-releasing hormone （GnRH）， follicle-stimulating hormone （FSH） and luteinizing hormone （LH） were measured. The insulin resistance indexes were calculated， and the ovary coefficients of rats were calculated. The pathological changes of ovary were observed. The protein and mRNA expressions of liver kinase B1 （LKB1） and AMP-activated protein kinase （AMPK） in ovary tissue were detected.

RESULTS

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Compared with normal group， the levels of blood glucose， insulin， insulin resistance index， serum levels of T， GnRH and LH and ovarian indexes were significantly increased （

P

＜0.05）， while serum levels of E

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and FSH as well as protein and mRNA expressions of LKB1 and AMPK in ovary tissue were decreased significantly （

P

＜0.05）； collagenization of ovarian cortex， increased number of atresia follicles and cystic follicles without cumulus， and follicular cystic lesions could be seen. Compared with model group， most of above indexes of Jinkui shenqi pills groups were reversed significantly （

P

＜0.05）； the number of follicle at each level was increased and no follicular cystic lesion was found in Jinkui shenqi pills medium-dose and high-dose groups.

CONCLUSIONS

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Jinkui shenqi pills can significantly improve the abnormal level of sex hormones， insulin resistance and ovarian cystic changes， the mechanism of which may be related to up-regulating the activation of LKB1/AMPK signaling pathway.