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Abstract
Background: Restenosis after airway stenting needs to be addressed urgently. Rapamycin has been proven to inhibit restenosis elsewhere. This study aimed at observing its effects on the respiratory tract. Methods: CCK-8, wound healing, Transwell and apoptosis assays were performed to detect the effects of rapamycin on the survival, migration, and apoptosis, respectively, of human tracheal fibroblasts (HTrF) and human tracheal epithelial cells (HTEpiC). Results: The effective concentrations of paclitaxel, mitomycin C and rapamycin on HTrF were 10−7–10−4 mol/L, 10−6–10−4 mol/L, and 10−5–10−4 mol/L, respectively. At the effective concentrations, the inhibition rates of paclitaxel on HTEpiC were (43.03 ± 1.12)%, (49.49 ± 0.86)%, (55.22 ± 1.43)%, and (93.19 ± 0.45)%; the inhibition rates of mitomycin C on HTEpiC were (88.11 ± 0.69)%, (93.82 ± 0.96)%, and (94.94 ± 0.54)%; the inhibition rates of rapamycin on HTEpiC were (10.19 ± 0.35)% and (94.55 ± 0.71)%. At the concentration of (1–4) × 10−5 mol/L, the inhibition rate of rapamycin on HTrF was more than 50%, and that on HTEpiC was less than 20% (p < 0.05). Conclusions: Compared to paclitaxel and mitomycin C, rapamycin had the least effect on HTEpiC while effectively inhibiting HTrF. The optimum concentration range was (1–4) × 10−5 mol/L.
Highlights
The treatment of benign cicatricial airway stenosis (BCAS) has always been a difficult problem in the field of respiratory intervention medicine
Paclitaxel, mitomycin C, and rapamycin at different concentrations and action times could inhibit the proliferation of human tracheal fibroblasts (HTrF) to varying degrees (Table 1)
The effective concentration of rapamycin with an inhibition rate of more than 50% on fibroblasts was 10−5 –10−4 mol/L (Figure 1C)
Summary
The treatment of benign cicatricial airway stenosis (BCAS) has always been a difficult problem in the field of respiratory intervention medicine. For patients with BCAS that cannot be treated with conventional interventional therapy and surgery, airway stent implantation is the only option. The destruction of airway mucosa by airway lesions, (2) the injury to the airway mucosa by interventional therapy [5], and (3) the continuous irritation of the airway mucosa by the airway stent. These factors activate the inflammation, promote the excessive proliferation of fibroblasts and the formation of cicatricial tissue, and lead to restenosis [5,6,7,8]. Complete epithelialization of the airway is key to preventing restenosis after stenting [9,10,11,12,13]
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