OBJECTIVE：To study the protective effect of timosaponin BⅡ（TB-Ⅱ）on blood vessels and explore its possible mechanism. METHODS ：Using aquaculture water as blank control ，the effects of 100，200 and 400 μg/mL TB-Ⅱ treatment for 48 h on the situation of subintestinal veins （SIVs）in normal zebrafish embryos 24 h after fertilization （24 hpf）were investigated. PTK787（0.06 μg/mL），a tyrosine kinase inhibitor ，was used to induce the model of zebrafish intestinal vascular injury ；using combing with 0.1％ dimethyl sulfoxide but no PTK 787 as blank control ，combing with PTK 787 but no drug as model control ，the effects treatment of 100，200 and 400 μg/mL TB-Ⅱ for 48 h on the SIVs of zebrafish model with vascular injury were investigated. Relative expressions of fam-like tyrosine kinase 1（Flt-1），kinase insert domain containing receptor （Kdr），kinase insert domain containing receptor l （Kdr-l），vascular endothelial growth factor A （VEGF-A），tumor necrosis factor α（TNF-α）and interleukin 6 （IL-6）mRNA were detected by RT-PCR. RESULTS ：100 μg/mL TB-Ⅱ could significantly increase the sprouting vessel of normal zebrafish SIVs sprouting vessel number （P＜0.05），and 200 μg/mL TB-Ⅱ could significantly increase SIVs number of normal zebrafish （P＜0.05）. Compared with blank control ， SIVs treatment （P＜0.01），and the relative expressions of Flt-l ， Kdr，Kdr-l，VEGF-A，TNF-α and IL-6 mRNA were alse decreased significantly （P＜0.05 or P＜0.01）. After treated 化。E-mail：pn333@163.com with different concentrations of TB- Ⅱ ，SIVs number of vascular injury model zebrafish increase d to different extents ；relative expressions of Flt-l ，Kdr，Kdr-l，VEGF-A，TNF-α and IL-6 mRNA were increased to different extents. There was no significant difference in SIVs number and the expression of Flt-l ，TNF-α mRNA in zebrafish treated with 100 μg/mL TB-Ⅱ and the expression of TNF-α mRNA in zebrafish treated with 400 μg/mL TB-Ⅱ， but there was statistical significance in other indexes （P＜0.05 or P＜0.01）. CONCLUSIONS ：TB-Ⅱ has a certain function of promoting angiogenesis and repairing damaged blood vessels ，and its mechanism is related to the up-regulation of vascular endothelial growth factor receptor and pro-inflammatory cytokine expression.