OBJECTIVE: To investigate the effect of local application of paclitaxel on airway scar formation after airway injury in rabbits. METHODS: Forty New Zealand rabbits were randomly divided into four groups, negative control group (n = 10), saline control group (n = 10), group I (n = 10), group II (n = 10). All rabbits received tracheotomy. In negative control group, the specimens were harvested for histological examination and immunohistochemical analysis immediately after tracheotomy;in other three groups, rabbits received airway injury after tracheotomy. In group I and group II, 0.4 mg/ml and 1.0 mg/ml paclitaxel was applied locally in injured airway segment for 3 minutes after airway injury. The normal saline was used in control group for 3 minutes. The animals were killed in 21 days after operation. The specimens were harvested for histological examination and immunohistochemical analysis. Transmission electron microscopy was employed to observe the ultrastructure of paclitaxel-induced apoptotic cells. RESULTS: The degree of stenosis in group I and group II were significantly decreased compared to those in saline control group [saline control group (59 ± 13)%, group I (27 ± 8)%, group II (22 ± 7)%]. Histological examination showed fibroblast cells and inflammatory cells in group I and group II were significantly fewer than in saline control group. The TGF-β1 positive cells and VEGF positive cells in group I and group II were significantly decreased compared to those in saline control group (P < 0.05). Paclitaxel-induced cell apoptosis and injured cell organs were observed by transmission electron microscopy. CONCLUSIONS: Local application of paclitaxel inhibits airway scar formation after airway injury in rabbit model, and the inhibition is dose dependent. Paclitaxel may have a therapeutic potential for the treatment of airway stenosis caused by endotracheal intubation, tracheotomy or implantation of airway stents.
OBJECTIVE: To investigate the effect of local application of paclitaxel on airway scar formation after airway injury in rabbits. METHODS: Forty New Zealand rabbits were randomly divided into four groups, negative control group (n = 10), saline control group (n = 10), group I (n = 10), group II (n = 10). All rabbits received tracheotomy. In negative control group, the specimens were harvested for histological examination and immunohistochemical analysis immediately after tracheotomy;in other three groups, rabbits received airway injury after tracheotomy. In group I and group II, 0.4 mg/ml and 1.0 mg/ml paclitaxel was applied locally in injured airway segment for 3 minutes after airway injury. The normal saline was used in control group for 3 minutes. The animals were killed in 21 days after operation. The specimens were harvested for histological examination and immunohistochemical analysis. Transmission electron microscopy was employed to observe the ultrastructure of paclitaxel-induced apoptotic cells. RESULTS: The degree of stenosis in group I and group II were significantly decreased compared to those in saline control group [saline control group (59 ± 13)%, group I (27 ± 8)%, group II (22 ± 7)%]. Histological examination showed fibroblast cells and inflammatory cells in group I and group II were significantly fewer than in saline control group. The TGF-β1 positive cells and VEGF positive cells in group I and group II were significantly decreased compared to those in saline control group (P < 0.05). Paclitaxel-induced cell apoptosis and injured cell organs were observed by transmission electron microscopy. CONCLUSIONS: Local application of paclitaxel inhibits airway scar formation after airway injury in rabbit model, and the inhibition is dose dependent. Paclitaxel may have a therapeutic potential for the treatment of airway stenosis caused by endotracheal intubation, tracheotomy or implantation of airway stents.