Department of Orthopedics, The Second Affiliated Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410012, P.R. China.
Orthopedic Institute, Clinical Medical College of Yangzhou University, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu 225001, P.R. China.
Mol Med Rep. 2019 Apr;19(4):2680-2686. doi: 10.3892/mmr.2019.9927. Epub 2019 Feb 1.
10‑Hydroxycamptothecin (HCPT) effectively controls epidural fibrosis, but the exact underlying mechanisms remain ambiguous. Abnormal microRNA (miR)‑23b‑3p expression has been detected in various types of fibrotic tissues that are present in different diseases. The aim of the present study was to elucidate the mechanisms through which HCPT induces fibroblast apoptosis. Reverse transcription‑quantitative polymerase chain reactions were performed on six traumatic scar samples and matched normal skin samples; traumatic scar formation was revealed to be significantly inversely associated with miR‑23b‑3p expression. In addition, the miR‑23b‑3p expression level in human fibroblasts was examined following HCPT treatment. The effects of HCPT and miR‑23b‑3p on fibroblast apoptosis were assessed using terminal deoxynucleotidyl‑transferase‑mediated dUTP nick‑end labeling, flow cytometry and western blot analysis. The results demonstrated that HCPT treatment notably increased miR‑23b‑3p expression levels and accelerated fibroblast apoptosis. Therefore, upregulation of miR‑23b‑3p expression was demonstrated to promote fibroblast apoptosis, consistently with the effects of HCPT. The results of the present study indicated that HCPT may induce fibroblast apoptosis by regulating miR‑23b‑3p expression.
10-羟基喜树碱（HCPT）能有效控制硬膜外纤维化，但确切的潜在机制仍不清楚。异常的 microRNA（miR）-23b-3p 表达已在存在于不同疾病中的各种类型的纤维化组织中被检测到。本研究旨在阐明 HCPT 诱导成纤维细胞凋亡的机制。对 6 个创伤性瘢痕样本和匹配的正常皮肤样本进行逆转录定量聚合酶链反应；创伤性瘢痕形成与 miR-23b-3p 的表达呈显著负相关。此外，还检测了 HCPT 处理后人成纤维细胞中 miR-23b-3p 的表达水平。采用末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记法、流式细胞术和 Western blot 分析评估 HCPT 和 miR-23b-3p 对成纤维细胞凋亡的影响。结果表明，HCPT 处理显著增加了 miR-23b-3p 的表达水平并加速了成纤维细胞凋亡。因此，上调 miR-23b-3p 的表达促进了成纤维细胞凋亡，与 HCPT 的作用一致。本研究结果表明，HCPT 可能通过调节 miR-23b-3p 的表达来诱导成纤维细胞凋亡。
