Current drug targets · 2026
Research on the Anti-breast Hyperplasia Mechanism of Liqi Sanjie Granules Based on Network Pharmacological Analysis and Experimental Verification.
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Hu Xionghui, Liu Xun, Yan Rensong, Li Xianhai, Zhou You, Chen Fei, Xu Min, Xiao Cheng, Wang Yi, Wang Zhang, Liu Yao, Zhong Bingguang, Hu Xiaoqi, Zhou Qing, Wei Tanjun
Аннотация
BACKGROUND: Breast hyperplasia has become a major public health challenge due to changes in dietary patterns. However, there is still a lack of effective pharmacotherapy for Breast hyperplasia.
METHODS: The chemical components of Liqi Sanjie Granules (LSG) were quantified through HPLC. Three key components were screened out by combining network pharmacology methods and experimental determination methods, whereas key components in sera were quantified through LC-MS. The potential molecular mechanisms of LSG and these three blood-entering chemicals for the treatment of breast hyperplasia were predicted by network pharmacology. Estradiol benzoate and progesterone were injected intramuscularly to establish a breast hyperplasia model. Serum estradiol (E2), progesterone (P), testosterone (T), and prolactin (PRT) were detected by ELISA. H&E was used in monitoring the hyperplasia of rat mammary gland tissues. Immunohistochemistry and RT-PCR were used to detect the protein and mRNA expression levels of estrogen receptors (ERs) and progesterone receptors (PR) in rat mammary glands.
RESULTS: The contents of seven components in LSG were quantified. After administration, the levels of paeoniflorin, glycyrrhizin, and ferulic acid were 280.16 ± 64.77, 101.87 ± 7.88, and 253.28 ± 17.64 μg per 200 μL, respectively. Network pharmacology studies have shown that LSG treats breast hyperplasia by acting on 63 targets in 36 signaling pathways, and the blood-entering chemicals of LSG involve 18 potential targets and 5 signaling pathways. Histopathological analysis revealed that rats in the LSG group had fewer mammary lobules and acini. Additionally, the proliferation of glandular epithelial cells was reduced. No significant changes were found in the serum levels of E2, P, PRT, and T in the LSG group. Concurrently, LSG can reduce the expression levels of PR protein and the mRNA of ESR1 and PGR in the rat mammary glands.
DISCUSSION: This study suggests that the blood-entering chemicals paeoniflorin, glycyrrhizin, and ferulic acid may alleviate breast hyperplasia through decreasing the expression levels of ER, ESR1, and PGR in the mammary tissues, reducing the number of mammary lobules and alveoli, and inhibiting pathological changes in vacuolar degeneration, hyperplasia, and detachment of glandular epithelial cells.
CONCLUSIONS: This study quantitatively analysed the seven chemical components of LSG and determined the contents of paeoniflorin, glycyrrhizin, and ferulic acid in the medicated serum. Furthermore, it demonstrates that LSG improves breast hyperplasia by regulating ER and PR expression levels.
METHODS: The chemical components of Liqi Sanjie Granules (LSG) were quantified through HPLC. Three key components were screened out by combining network pharmacology methods and experimental determination methods, whereas key components in sera were quantified through LC-MS. The potential molecular mechanisms of LSG and these three blood-entering chemicals for the treatment of breast hyperplasia were predicted by network pharmacology. Estradiol benzoate and progesterone were injected intramuscularly to establish a breast hyperplasia model. Serum estradiol (E2), progesterone (P), testosterone (T), and prolactin (PRT) were detected by ELISA. H&E was used in monitoring the hyperplasia of rat mammary gland tissues. Immunohistochemistry and RT-PCR were used to detect the protein and mRNA expression levels of estrogen receptors (ERs) and progesterone receptors (PR) in rat mammary glands.
RESULTS: The contents of seven components in LSG were quantified. After administration, the levels of paeoniflorin, glycyrrhizin, and ferulic acid were 280.16 ± 64.77, 101.87 ± 7.88, and 253.28 ± 17.64 μg per 200 μL, respectively. Network pharmacology studies have shown that LSG treats breast hyperplasia by acting on 63 targets in 36 signaling pathways, and the blood-entering chemicals of LSG involve 18 potential targets and 5 signaling pathways. Histopathological analysis revealed that rats in the LSG group had fewer mammary lobules and acini. Additionally, the proliferation of glandular epithelial cells was reduced. No significant changes were found in the serum levels of E2, P, PRT, and T in the LSG group. Concurrently, LSG can reduce the expression levels of PR protein and the mRNA of ESR1 and PGR in the rat mammary glands.
DISCUSSION: This study suggests that the blood-entering chemicals paeoniflorin, glycyrrhizin, and ferulic acid may alleviate breast hyperplasia through decreasing the expression levels of ER, ESR1, and PGR in the mammary tissues, reducing the number of mammary lobules and alveoli, and inhibiting pathological changes in vacuolar degeneration, hyperplasia, and detachment of glandular epithelial cells.
CONCLUSIONS: This study quantitatively analysed the seven chemical components of LSG and determined the contents of paeoniflorin, glycyrrhizin, and ferulic acid in the medicated serum. Furthermore, it demonstrates that LSG improves breast hyperplasia by regulating ER and PR expression levels.