This study was aimed to observe the influence on angiogenesis factor and expression of its receptor protein on estrogen-induced uterine fibroids rat models with Y i-Qi Xiao-Zheng (YQXZ) method, in order to explore the mechanism of this method in the inhibition of angiogenesis in the treatment of uterine fibroids. Castration and estro-gen-induced method were used in the establishment of guinea pig uterine fibroids rat model. And then, different doses of Chinese medicine of YQXZ method were given. The immunohistochemical method was used in the detection of microvessel density (MVD) and vascular endothelial growth factor (VEGF) protein expression of the uterine tissues. The RT-PCR method was used to detect the expression of VEGFR1 mRNA and VEGFR2 mRNA. Then, statistical analysis was given on indexes mentioned above. The results showed that compared with the normal control group, ex-pression of MVD, VEGF and VEGFR of uterine muscle tissues in the model group was significantly higher (P <0.01). Compared with the model group, Chinese medicine group of different doses showed different reducing. Among them, the high-dose group was the most obvious one. It showed that the high-dose Chinese medicine of YQXZ group was able to significantly inhibit the expression of MVD, VEGF and theirs receptors. It was concluded that YQXZ method can antagonize proliferation of the leiomyoma cell by inhibiting angiogenesis. Therefore, it may be one of the mechanisms of this method in the treatment of uterine fibroids.

BACKGROUD: Coronary artery disease (CAD), a common disease with high incidence and mortality rate, has seriously threatened the health and life of the public. Traditional Chinese medicine (TCM) has an important role in the prevention and treatment of this disease. Through clinical epidemiological survey, a deeper understanding of TCM etiology and syndrome characteristics in CAD would further improve clinical efficacy in the treatment of this disease.

OBJECTIVE To study the improvement effect and mechanism of Shuhou tongqi formula on intestinal injury in mice with postoperative ileus （POI）. METHODS Mice were randomly divided into sham operation group， model group， positive control group （Mosapride citrate tablets， 1.95 mg/kg）， and Shuhou tongqi formula group （1.88 g/kg）， with 6 mice in each group. Except for the sham operation group， POI model was induced in other groups by typical small intestinal interference. Each group was given relevant drug liquid/water， once a day， for consecutive 2 days. After the last medication， the percentage of carbon powder propulsion in small intestine was detected， and pathomorphological changes in ileum tissue of mice were observed. The serum levels of interleukin-6 （IL-6）， IL-10， tumor necrosis factor-α （TNF-α）， motilin （MTL） and somatostatin （SS） were all detected； the expression levels of Toll-like receptor 4 （TLR4）， nuclear factor κB （NF-κB p65） and p38 mitogen-activated protein kinase （p38 MAPK） were determined in ileal tissue of mice； the gut microbiota of colon contents was analyzed in each group of mice. RESULTS After the intervention of Shuhou tongqi formula， pathological damage such as intestinal wall atrophy and mucosal capillary congestion in ileum tissue were improved significantly； the percentage of carbon powder propulsion and the serum level of IL-10 and MTL were increased significantly （P＜0.05）； however， serum levels of TNF-α， IL-6 and SS， the expressions of TLR4， NF-κB p65 and p38 MAPK were decreased significantly （P＜0.05）. The analysis of gut microbiota showed that Shuhou tongqi formula could significantly increase ACE， Chao1， Shannon and PD indexes， and relative abundance of Akkermansia （P＜0.05）， but decreased relative abundance of Proteobacteria， Ligilactobacillus and Escherichia-Shigella significantly （P＜0.05）. CONCLUSIONS Shuhou tongqi formula can improve intestinal injury and inflammatory reaction of POI mice， the mechanism of which may be associated with inhibiting the activity of TLR4/ NF-κB/MAPK signaling pathway， regulating the levels of gastrointestinal hormones and improving the disturbance of intestinal flora in mice. E-mail：1643589936@qq.com