Effects of Stellera chamaejasme on microvascular density and apoptosis of cancer cells in a rat bladder tumor model

Background: Investigate the effects of Stellera chamaejasme on microvascular density and apoptosis of cancer cells in rat bladder tumor models. Methods: The bladder tumor model of 75 specific pathogen-free (SPF)-grade Sprague-Dawley (SD) rats aged 5-6 weeks was established by n-methyl-N-nitrosourea (MNU) bladder perfusion induction, and the model rats were randomly divided into model group, low-dose (L-dose) group, medium-dose (M-dose) group, high-dose (H-dose) group, and positive drug (HCPT) group. L-dose group, M-Dose group, and H-dose group were treated with 5 g/kg, 10 g/kg, and 20 g/kg, respectively. The HCPT group was treated with 2 mg/kg hydroxycamptothecin at 1 mL/kg once a week and the model group were treated with the same amount of normal saline for 4 weeks. The quality of bladder cancer tissues in each group was measured. The pathological changes and microvascular density of bladder tissues were observed, and the apoptosis rate of vascular endothelial growth factor (VEGF), tumor tissue and the protein expression levels of factor associated suicide (Fas), factor associated suicide ligand (FasL) and Caspase3 in bladder tissues were detected. Results: Bladder cancer was induced 14 weeks after initial bladder perfusion with MNU. In the model group, epithelial cells of bladder tissue showed atypically hyperplasia with various sizes and disorders. After treatment with Stellera chamaejasme, the hematoxylin-eosin (HE) scores, bladder weight, microvascular density, and VEGF were significantly decreased, and the tumor inhibition rate, cell apoptosis, and the expression of apoptosis-related proteins Fas, FasL, and Caspase3 were significantly increased in the bladder tissue. The above changes were dose-dependent with Stellera chamaejasme. Conclusions: MNU can be used to prepare a rat bladder cancer model. Stellera chamaejasme has a good therapeutic effect on rat bladder cancer, which may inhibit the progression of bladder cancer by inhibiting micro-angiogenesis and inducing the apoptosis of bladder tumor cells.