Department of Otolaryngology-Head & Neck Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232-8605, USA.
Otolaryngol Head Neck Surg. 2012 Aug;147(2):302-7. doi: 10.1177/0194599812440419. Epub 2012 Mar 7.
To investigate the hypothesis that prophylactic triamcinolone modulates acute vocal fold inflammatory and profibrotic signaling during acute phonotrauma.
In vivo rabbit phonation model.
Academic medical center.
Forty New Zealand white breeder rabbits were randomly assigned to 1 of 4 groups: control (no intervention), no treatment (30 minutes of raised intensity phonation), sham treatment (bilateral intralaryngeal triamcinolone acetonide injection at 0 µg/25 µL followed by 30 minutes of raised intensity phonation), or steroid treatment (bilateral intralaryngeal triamcinolone acetonide injection at 400 µg/25 µL followed by 30 minutes of raised intensity phonation). Quantitative polymerase chain reaction (qPCR) was used to investigate gene expression levels of cyclooxygenase-2 (COX-2), interleukin (IL)-1β, and transforming growth factor (TGF)-β1.
Results revealed a significant main effect for COX-2 (P = .002). Post hoc testing revealed that rabbits receiving no treatment (15.10) had higher COX-2 gene expression than control (5.90; P < .001). There were no significant differences in COX-2 expression between treatment groups. Results revealed a significant main effect for IL-1β (P < .001). Post hoc testing revealed that rabbits receiving no treatment (14.70) had higher IL-1β gene expression than control (6.30) (P = .001). There were no significant differences in IL-1β gene expression between treatment groups. There were no significant differences in TGF-β1 gene expression (P = .525) between treatment and control groups.
Given conflicting evidence, further studies are necessary to investigate vocal fold steroid injections prior to and following the induction of phonotrauma. Prophylactic administration of triamcinolone immediately prior to acute phonotrauma resulted in no significant changes in COX-2, IL-1β, and TGF-β1 gene transcript levels.
研究预防性曲安奈德在急性声创伤期间调节急性声带炎症和纤维化信号的假说。
体内兔发声模型。
学术医疗中心。
40 只新西兰白种繁殖兔随机分为 4 组之一：对照组（无干预）、无治疗组（30 分钟提高强度发声）、假治疗组（双侧喉内曲安奈德丙酮注射 0µg/25µL 后进行 30 分钟提高强度发声）或类固醇治疗组（双侧喉内曲安奈德丙酮注射 400µg/25µL 后进行 30 分钟提高强度发声）。使用定量聚合酶链反应（qPCR）来研究环氧化酶-2（COX-2）、白细胞介素（IL）-1β和转化生长因子（TGF）-β1的基因表达水平。
结果显示 COX-2 有显著的主效应（P=0.002）。事后检验显示，未接受治疗的兔子（15.10）的 COX-2 基因表达高于对照组（5.90；P<0.001）。治疗组之间的 COX-2 表达无显著差异。结果显示 IL-1β 有显著的主效应（P<0.001）。事后检验显示，未接受治疗的兔子（14.70）的 IL-1β 基因表达高于对照组（6.30）（P=0.001）。治疗组之间的 IL-1β 基因表达无显著差异。TGF-β1 基因表达在治疗组和对照组之间无显著差异（P=0.525）。
鉴于证据相互矛盾，有必要进一步研究在声创伤诱导前后进行声带类固醇注射。在急性声创伤前立即预防性给予曲安奈德，不会导致 COX-2、IL-1β 和 TGF-β1 基因转录水平发生显著变化。
