Objective To explore the effect and mechanism of Kuntai Capsule (KC) on premature ovarian failure in rats.Methods Totally 40 SD female rats were randomly divided into four groups:control group,model group,Kuntai Capsule (KC) group and conjugated estrogens tablets (CET) group.The premature ovarian failure model in rats was made by ig administration of 75 mg/kg tripterygium.After the model was established,rats were continually treated with 0.6 and 0.625 g/kg of KC and CET respectively by ig administration for 36 d.HE staining was used to observe the morphology of ovary and count the number of follicle.The enzyme-linked immunosorbent assay (Elisa) method was used for the detection of follicle stimulating hormone (FSH),luteinizing hormone (LH),serum estradiol (E2),and anti-Mueller tube hormone (AMH) level.The real-time fluorescence quantitative PCR (qRT-PCR) method was used to detect the mRNA expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF).Results Compared with control group,the number of primordial follicles,preantral follicles and antral follicles were significantly reduced,the number of atretic follicles was increased (P ＜ 0.05),E2 and AMH significantly decreased (P ＜ 0.05),FSH and LH levels increased significantly (P ＜ 0.05),and the levels of VEGF and bFGF mRNA in model group were significantly decreased (P ＜ 0.05).Compared with model group,the number of primordial follicles,preantral follicles,and antral follicles were significantly increased,the number of atretic follicles was significantly reduced (P ＜ 0.05),E2 and AMH significantly increased (P ＜ 0.05),FSH and LH levels significantly decreased (P ＜ 0.05),and the levels of VEGF and bFGF mRNA in KC group were significantly increased (P ＜ 0.05).Conclusion By regulating the level of hormone and up-regulating the expression of VEGF and bFGF,KC can repair the damaged ovarian tissue and promote the growth and development of the follicle,so as to inhibit the premature exhaustion of mRNA.

Coronary artery disease (CAD) is a chronic disease but causes the highest mortality and morbidity among the cardiovascular diseases worldwide. Correlations between CAD and gut microbiota have been observed. This suggests that the gut microbiota could become a vital diagnostic marker of CAD, and restoring the gut habitat may become a promising strategy for CAD therapy. The elevated level of trimethylamine-N-oxide (TMAO), a gut microbiota-derived metabolite, was found to be associated with the increased risk of cardiovascular disease and the all-cause mortality. Preclinical studies have shown that it has pro-arteriosclerosis properties. It is likely that regulating the production of TMAO by gut microbiota may become a promising strategy for anti-atherosclerosis therapy. This review summarizes the clinical and preclinical researches on the intervention of CAD by regulating the gut microbiota and the microbiota-derived metabolite TMAO, with the aim to provide new target for the therapy of CAD.
Coronary Artery Disease ; Gastrointestinal Microbiome ; Humans ; Methylamines ; Oxides