Department of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität Düsseldorf, Moorenstr.5, Düsseldorf, 40225, Germany.
Department of Neurosurgery, University Hospital Helsinki, Topeliuksenkatu 5, Helsinki, 00260, Finland.
Cell Commun Signal. 2024 Apr 3;22(1):214. doi: 10.1186/s12964-024-01594-x.
Smoking is the major cause of cardiovascular diseases and cancer. It induces oxidative stress, leading to DNA damage and cellular senescence. Senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase, which are known to play a vital role in the initiation and progression of cardiovascular diseases and metastasis in cancer. The current study investigated the smoking induced cellular senescence and employed colchicine that blocked senescence in endothelial cells exposed to tobacco smoke condensate. Colchicine prevented oxidative stress and DNA damage in tobacco smoke-condensate-treated endothelial cells. Colchicin reduced β-gal activity, improved Lamin B1, and attenuated cell growth arrest markers P21 and P53. Colchicine also ameliorated the expression of SASP factors and inhibited the activation of NF-kB and MAPKs P38 and ERK. In summary, colchicine inhibited tobacco smoke condensate-induced senescence in endothelial cells by blocking the activation of NF-kB and MAPKs P38 and ERK.
吸烟是心血管疾病和癌症的主要原因。它会引起氧化应激，导致 DNA 损伤和细胞衰老。衰老细胞会增加促炎分子和基质金属蛋白酶的表达和释放，这些分子和蛋白酶已知在心血管疾病的发生和进展以及癌症的转移中起着至关重要的作用。本研究调查了吸烟引起的细胞衰老，并使用秋水仙碱阻断暴露于烟草烟雾凝结物的内皮细胞中的衰老。秋水仙碱可预防烟草烟雾凝结物处理的内皮细胞中的氧化应激和 DNA 损伤。秋水仙碱降低了β-半乳糖苷酶的活性，改善了核纤层蛋白 B1，并减弱了细胞生长抑制标记物 P21 和 P53。秋水仙碱还改善了 SASP 因子的表达，并抑制了 NF-kB 和 MAPKs P38 和 ERK 的激活。总之，秋水仙碱通过阻断 NF-kB 和 MAPKs P38 和 ERK 的激活来抑制内皮细胞中烟草烟雾凝结物诱导的衰老。
