Li Shasha, Ren Liwen, Jia Di, Yang Dan, Hao Lijun
From the Plastic and Cosmetic Center, The First Affiliated Hospital of Harbin Medical University; Department of Biochemistry, Qiqihar Medical University; and Teaching and Research Department of Biochemistry and Molecular Biology, Harbin Medical University.
Plast Reconstr Surg. 2022 Oct 1;150(4):815-826. doi: 10.1097/PRS.0000000000009574. Epub 2022 Jul 27.
Capsular contracture is a serious complication that occurs after augmentation mammaplasty. The authors previously identified that carboxymethyl chitin had an inhibitory effect on capsule formation. This study was performed to elucidate the possible molecular mechanisms through which carboxymethyl chitin inhibits the formation of a capsule around silicone implants.
In this study, the authors cultured human dermal fibroblasts and treated them with carboxymethyl chitin in vitro. The difference in proliferation between treated and untreated cells was analyzed through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Protein levels of transforming growth factor beta-1 and alpha smooth muscle actin (α-SMA) were examined by Western blot analysis. Expression levels of type I and type III collagen were checked by enzyme-linked immunosorbent assay. In vivo, silicone implants were placed under the pectoralis muscle in 12 female rabbits. The thickness of the capsule was measured by histologic analysis, and the effect of carboxymethyl chitin on α-SMA, collagen type I and III expression levels was evaluated by real-time polymerase chain reaction analysis, enzyme-linked immunosorbent assay, Western blot, and immunofluorescence analysis.
In the in vitro study, we confirmed that carboxymethyl chitin inhibited the proliferation of fibroblasts. The protein expression levels of collagen type I, transforming growth factor beta-1, and α-SMA were inhibited by carboxymethyl chitin treatment. In vivo, carboxymethyl chitin treatment reduced capsular thickness and the expression of α-SMA and collagen types I and III in capsules around silicone implants.
The authors' results showed that carboxymethyl chitin could influence capsule formation around silicone implants by inhibiting the fibroblast activity, interrupting fibroblast-to-myofibroblast differentiation, and decreasing collagen synthesis.
Carboxymethyl chitin influence capsule formation around silicone implants. Although more clinical studies are needed to verify the effect of carboxymethyl chitin on capsular contracture, the authors believe that it will play an effective role in the clinical application of reducing the occurrence of capsular contracture.
包膜挛缩是隆乳术后发生的一种严重并发症。作者之前已确定羧甲基壳聚糖对包膜形成有抑制作用。本研究旨在阐明羧甲基壳聚糖抑制硅胶植入物周围包膜形成的可能分子机制。
在本研究中,作者体外培养人真皮成纤维细胞并用羧甲基壳聚糖处理。通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐法分析处理组和未处理组细胞之间的增殖差异。通过蛋白质印迹分析检测转化生长因子β-1和α平滑肌肌动蛋白(α-SMA)的蛋白水平。通过酶联免疫吸附测定法检查I型和III型胶原蛋白的表达水平。在体内,将硅胶植入物置于12只雌性兔的胸大肌下方。通过组织学分析测量包膜厚度,并通过实时聚合酶链反应分析、酶联免疫吸附测定法、蛋白质印迹和免疫荧光分析评估羧甲基壳聚糖对α-SMA、I型和III型胶原蛋白表达水平的影响。
在体外研究中,我们证实羧甲基壳聚糖抑制成纤维细胞的增殖。羧甲基壳聚糖处理可抑制I型胶原蛋白、转化生长因子β-1和α-SMA的蛋白表达水平。在体内,羧甲基壳聚糖处理可降低硅胶植入物周围包膜的厚度以及包膜中α-SMA和I型和III型胶原蛋白的表达。
作者的结果表明,羧甲基壳聚糖可通过抑制成纤维细胞活性、中断成纤维细胞向肌成纤维细胞的分化以及减少胶原蛋白合成来影响硅胶植入物周围的包膜形成。
羧甲基壳聚糖影响硅胶植入物周围的包膜形成。尽管需要更多的临床研究来验证羧甲基壳聚糖对包膜挛缩的作用,但作者认为它将在减少包膜挛缩发生的临床应用中发挥有效作用。