Mechanism of Jianpi huatan formula improving polycystic ovary syndrome in rats by regulating the HMGB1/RAGE signaling pathway
- VernacularTitle:健脾化痰方调控HMGB1/RAGE通路改善大鼠多囊卵巢综合征的机制研究
- Author:
Jing XU
1
;
Ying XIANG
1
Author Information
1. Dept. of Obstetrics and Gynecology，Guanggu Branch，Hubei Provincial Hospital of TCM/Hubei Provincial Key Laboratory of Research and Application of TCM for Liver and Kidney Diseases，Wuhan 430070，China
- Publication Type:Journal Article
- Keywords:
Jianpi huatan formula;
polycystic ovary syndrome;
HMGB1/RAGE signaling pathway;
insulin resistance
- From:
China Pharmacy
2026;37(8):1009-1014
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To explore the effects of the Jianpi huatan formula （JPHTF） on polycystic ovary syndrome （PCOS） in rats by regulating the high mobility group box 1 protein （HMGB1）/receptor for advanced glycation end products （RAGE） signaling pathway. METHODS The rats were randomly divided into the normal （Con） group， the PCOS group， the JPHTF-L group （5.54 g/kg）， the JPHTF-H group （11.07 g/kg）， the JPHTF-H+rHMGB1 group （11.07 g/kg of JPHTF+8 μg/kg of rHMGB1）， and metformin group （0.27 g/kg）， with 12 rats in each group. Except for the rats of Con group， which were given 1% sodium carboxymethyl cellulose intragastrically and fed with normal chow， the remaining rats were induced to develop PCOS models by using a high-fat diet combined with letrozole. Af ter successful modeling， rats in each drug group were administered the corresponding drugs by gavage or tail vein injection once a day for 4 consecutive weeks. 24 h after the intervention， body weight and ovarian coefficient were detected. The levels of fasting blood glucose （FBG）， serum levels of fasting insulin （FINS）， follicle stimulating hormone （FSH）， luteinizing hormone （LH）， testosterone （T） and estradiol （E 2 ） were detected. The homeostasis model assessment of insulin resistance （HOMA-IR） was calculated. The levels of tumor necrosis factor-α （TNF-α）， interleukin-18 （IL-18） and IL-1β and the protein expressions of HMGB1， RAGE， phosphorylated nuclear factor-κB （p-NF-κB） and NF-κB in the ovarian tissues of rats were detected. The morphology of ovarian tissue was observed， and the numbers of cystic follicles and corpora lutea were counted. RESULTS Compared with PCOS group， polycystic changes of ovarian tissue in rats showed varying degrees of improvement in the JPHTF-L group， JPHTF-H group， and metformin group； body weight， ovarian coefficient， FBG， the number of cystic follicles， serum levels of FINS， HOMA-IR， T， LH， LH/FSH， the levels of TNF-α， IL-18 and IL-1β and protein expressions of HMGB1 and RAGE in ovarian tissue as well as phosphorylation level of NF-κB protein all significantly decreased； the number of corpora lutea and the serum levels of E 2 and FSH significantly increased （ P ＜0.05）. Compared with JPHTF-H group， above indexes of rats were reversed significantly in JPHTF-H+rHMGB1 group （ P ＜0.05）. CONCLUSIONS JPHTF can reduce the inflammatory response in PCOS rats， mitigate ovarian injury， regulate hormone balance， and improve insulin resistance and follicular development by inhibiting the HMGB1/RAGE signaling pathway.
