Effects of dodder total flavone on polycystic ovary syndrome rat models induced by DHEA combined HCG

Abstract EN

Aims : Explore the effects of dodder total flavone on polycystic ovary syndrome (PCOS) rat models induced by dehydroepiandrosterone (DHEA) combined human chorionic gonadotropin (HCG).

Methods : Except the blank group, the rest of the rats were injected with DHEA 6 mg/100 g on the back of the neck and 1.5 IU HCG each day, for 21 consecutive days.

On the 16th day of modeling, vaginal smear was performed to select the model rats, which were randomly divided into model group, dacin-35 group, large, middle and small dose dodder total flavonoids groups, and given the medicine for three weeks.

At the end of the last administration, take samples, so as to calculate the ovaries and uterus indexes, measure serum LH / FSH ratio, P, PRL and INS levels, fixed the uterus and pancreas in 10% formalin solution and stained with HE to observe the morphological changes of the organs.

And measure the expression of TNFa and IGF-l proteins in ovaries by immunohistochemistry.

Results : Compared with the blank group, ovarian and uterine indexes, serum LH/FSH ratio, serum PRL and INS levels, ovary TNF-a and IGF-l protein expression were significantly increased, and significant pathological changes were observed in the uterine and pancreatic tissues in model group (P < 0.01).

While the serum P level decreased significantly (P < 0.01), Compared with the model group, the ovarian and uterine indexes, serum LH/FSH ratio, serum P, PRL and INS levels, ovary TNF-a protein expression were significantly decreased in large, middle and small dose dodder total flavonoids groups (P < 0.01); The expression of IGF-1 protein was decreased and uterus pathological changes were improved in different extents (P < 0.01 or P < 0.05), pancreas pathological changes were improved significantly (P < 0.01).

Conclusion: PCOS rat models was successfully replicated.

Dodder total flavone can protect PCOS rats induced by DHEA combined HCG by different action pathways.