Lan Yu-Jie, Yan Rong-Shuai, Lei Ze-Yuan, Fan Dong-Li
Department of Plastic and Cosmetic Surgery, Xinqiao Hospital, Army Medical University, Xinqiao Road, Sha Ping Ba District, Chongqing, 400037, People's Republic of China.
Aesthetic Plast Surg. 2024 Dec;48(24):5358-5366. doi: 10.1007/s00266-024-04323-4. Epub 2024 Aug 26.
Capsular contracture is one of the most severe complications following breast augmentation surgery. It has been reported that botulinum toxin Type A (BTX-A) can inhibit capsular contracture, but the exact mechanisms remain unclear. Therefore, this study aims to explore the potential mechanisms behind BTX-A's inhibition of capsular contracture by observing its effects on the biological behavior of fibroblasts and its impact on the TGF-β/Smad signaling pathway.
In vitro experiments involved culturing fibroblasts on PDMS surfaces, subsequently treating them with various concentrations of BTX-A. Fibroblast proliferation activity was assessed using the CCK-8 assay, while the migration and cytoskeletal morphology of the fibroblasts were meticulously examined. ELISA was utilized to quantify the expression of fibrosis-related cytokines. Gene and protein expressions related to the TGF-β/Smad pathway were analyzed through real-time PCR and Western blotting techniques.
BTX-A moderately enhanced the early proliferation and migration of fibroblasts on the surface of PDMS silicone sheets and reduced the synthesis of collagen types I and III. Furthermore, under the influence of BTX-A, the expression of TGF-βR2 and α-SMA in the TGF-β/Smad pathway was significantly inhibited.
This study demonstrates that BTX-A can inhibit fibroblast differentiation by downregulating the expression of TGF-βR2, thereby suppressing the TGF-β/Smad pathway. This suggests a possible mechanism through which BTX-A mitigates capsular contracture.
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包膜挛缩是隆胸手术后最严重的并发症之一。据报道，A型肉毒杆菌毒素（BTX-A）可抑制包膜挛缩，但其确切机制尚不清楚。因此，本研究旨在通过观察BTX-A对成纤维细胞生物学行为的影响及其对TGF-β/Smad信号通路的作用，探讨其抑制包膜挛缩的潜在机制。
体外实验包括在聚二甲基硅氧烷（PDMS）表面培养成纤维细胞，随后用不同浓度的BTX-A处理。使用CCK-8法评估成纤维细胞的增殖活性，同时仔细检查成纤维细胞的迁移和细胞骨架形态。采用酶联免疫吸附测定（ELISA）法对纤维化相关细胞因子的表达进行定量分析。通过实时聚合酶链反应（PCR）和蛋白质免疫印迹技术分析与TGF-β/Smad通路相关的基因和蛋白表达。
BTX-A适度增强了PDMS硅胶片表面成纤维细胞的早期增殖和迁移，并减少了I型和III型胶原蛋白的合成。此外，在BTX-A的作用下，TGF-β/Smad通路中TGF-βR2和α-SMA的表达受到显著抑制。
本研究表明，BTX-A可通过下调TGF-βR2的表达抑制成纤维细胞分化，从而抑制TGF-β/Smad通路。这提示了BTX-A减轻包膜挛缩的一种可能机制。
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