In fibrotic skeletal muscles, excessive extracellular matrix (ECM) deposition is a result of increased activation and decreased apoptosis of myofibroblasts. The aim of this study is to investigate whether treatment with quercetin, kaempferol or capsaicin can reduce the transforming growth factor-beta 1 (TGF-β1)-induced myofibroblast differentiation and fibrotic ECM expression in differentiated C2C12 cells. Two-day-differentiated C2C12 cells were treated with TGF-β1 for 48 h to induce myofibroblast differentiation. Twenty-four hours before (pre-treatment) and for forty-eight hours with (co-treatment) TGF-β1 treatment, cells were exposed to quercetin (25, 50 µM), kaempferol (10, 25, 50 µM) or capsaicin (25, 50 µM). The immunofluorescence intensity of alpha smooth muscle actin (αSMA) and collagen type I/III gene expression were assessed as myofibroblast markers. MyoD immunofluorescence intensity was measured as a myogenic marker. Co-treatment of TGF-β1 with the phytochemicals was most effective, resulting in a decreased number of αSMA-positive cells (all three compounds), decreased collagen type I (kaempferol, capsaicin) and type III (kaempferol) gene expression, and increased MyoD (kaempferol, capsaicin) protein expression compared to TGF-β1 treatment. This study demonstrates that treatment with quercetin, kaempferol or capsaicin can reduce myofibroblast markers. This suggests a possible anti-fibrotic effect of the phytochemicals in skeletal muscle.
Quercetin, Kaempferol and Capsaicin Counteract the TGF-β1-Induced Upregulation of αSMA and Collagen in Myoblasts.
槲皮素、山奈酚和辣椒素可拮抗 TGF-β1 诱导的成肌细胞中 αSMA 和胶原蛋白的上调
阅读:5
作者:Cuijpers Iris, Sthijns Mireille M J P E, van den Bogart Veerle A R, Katsburg Joey, Leenders Cliff F M, Troost Freddy J
| 期刊: | International Journal of Molecular Sciences | 影响因子: | 4.900 |
| 时间: | 2025 | 起止号: | 2025 May 27; 26(11):5151 |
| doi: | 10.3390/ijms26115151 | 研究方向: | 细胞生物学 |
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
