Lichong decoction inhibits micro-angiogenesis by reducing the expressions of hypoxia inducible factor-1α and vascular endothelial growth factor in hysteromyoma mouse model

• 作者: Wang Wenna Zhang Wufang Li Donghua Qian Ruiya Zhu Lijuan Liu Yu Chen Chao
• 来源期刊: 中医杂志（英文版）
• 年，卷（期）: 2020,（6）
• 所属期刊栏目: Research Articles
• 页码范围: 928-937
• 页数: 10页
• 语种: 英文

摘要

OBJECTIVE: To investigate the efficacy of Lichong decoction (LD) from Traditional Chinese Medicine,on micro-angiogenesis in a mouse model of hysteromyoma.METHODS: A mouse model of hysteromyoma was developed by orthotopic intrauterine injection of primary human myoma cells isolated from patients from the Beijing Obstetrics and Gynecology Hospital into CB-17 Scid mice.Mice were administered high-dose LD,low-dose LD,mifepristone or water (control) daily by gavage for 4 weeks.Uterine diameter and coefficient (uterine weight/body weight) were measured.Uterine morphology was assessed by light microscopy (hematoxylin and eosin) and transmission electron microscopy.Serum levels of estradiol,progesterone,follicle-stimulating hormone and luteinizing hormone (LH) were measured by enzyme-linked immunosorbent assay.Uterine protein expression of hypoxia inducible factor (HIF)-1α,CD31 and proliferating cell nuclear antigen (PCNA) was detected by immunohistochemistry.VEGF and HIF-1α mRNAs were quantified by RT-PCR.RESULTS: High-dose LD,low-dose LD and mifepristone reduced uterine diameter and coefficient,and attenuated the morphologic abnormalities associated with hysteromyoma.High-dose LD,low-dose LD and mifepristone inhibited hysteromyoma-induced micro-angiogenesis,as evidenced by a decrease in the number of new microvessels co-immunostaining for CD31 and PCNA (P ＜ 0.01).High-dose LD and mifepristone lowered serum levels of estradiol,progesterone and LH (P ＜ 0.05).High-dose LD,low-dose LD and mifepristone down-regulated HIF-1α mRNA and protein expressions and VEGF mRNA expression (P ＜ 0.01).CONCLUSION: The inhibition of hysteromyoma by LD may involve reductions in HIF-1α and VEGF expression and suppression of micro-angiogenesis.