生物学杂志

生物学杂志 ›› 2026, Vol. 43 ›› Issue (1): 79-.doi: 10.3969/j.issn.2095-1736.2026.01.079

• 研究报告 • 上一篇    下一篇

生长抑素信号通过抑制软骨内骨化来调节骨量

刘　璐1,2, 于　茜1,2, 袁辉明1,2， 陈　洁11,2
  

  1. 1. 上海海洋大学 国家海洋生物科学国际联合研究中心， 上海 201306；
    2. 上海海洋大学 水产种质资源发掘与利用教育部重点实验室， 上海 201306
  • 出版日期:2026-02-18 发布日期:2026-02-27
  • 通讯作者: 陈洁，博士，助理研究员，研究方向为鱼类内分泌，E-mail：chenjie@shou.edu.cn
  • 作者简介:刘璐，硕士，研究方向为鱼类内分泌，E-mail：958486896@qq.com
  • 基金资助:
    上海海洋大学水产一流学科支持项目（A1-3201-19-3020）

Somatostatin signaling regulates bone mass by inhibiting endochondral ossification

LIU Lu1,2, YU Qian1,2, YUAN Huiming1,2, CHEN Jie1,2   

  1. 1. International Research Center for Marine Biosciences, Shanghai Ocean University, Shanghai 201306, China;
    2. Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources, Ministry of Education,
    Shanghai Ocean University, Shanghai 201306, China
  • Online:2026-02-18 Published:2026-02-27

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摘要： 生长抑素（somatostatin, SST）是一种功能多样的肽，也是内分泌生长轴中的一类十分重要的调控因子，具有广泛的内分泌和外分泌功能，一些证据表明生长抑素（SST）可能在骨生理学中发挥作用。本研究旨在探究生长抑素信号通路在斑马鱼骨骼发育中的调控作用。通过Somatostatin1.2（sst1.2）基因敲除的斑马鱼模型，综合运用阿利新蓝软骨染色、茜素红硬骨染色、微型CT扫描、钙黄绿素标记以及关键成骨基因表达分析等多重技术手段评估SST信号对骨骼发育的影响。实验结果显示，sst1.2缺失未显著影响软骨发育和脊柱的膜内骨化过程，但使得斑马鱼突变体头骨骨量明显增加；鳞片发育未受干扰；组织学分析和成骨基因表达证实骨量增加源于软骨内骨化增强。以上结果揭示了在斑马鱼成骨过程中，SST信号通过抑制斑马鱼软骨内骨化进而调节骨量。这可为深入解析鱼类骨骼发育提供新的理论基础，也为建立更精准的骨骼发育异常疾病模型（如骨代谢障碍性疾病）开辟新思路。

关键词: 生长抑素, 骨量, 软骨内骨化, 斑马鱼, CRISPR/Cas9

Abstract: Somatostatin （SST）is a multifunctional peptide and an important regulator of the endocrine growth axis, exerting a wide range of endocrine and exocrine functions. Scattered evidence suggested a possible role for SST in bone physiology. The aim of this study was to investigate the regulatory role of growth inhibitor signaling pathway in zebrafish skeletal development. The effects of SST signaling on skeletal development were assessed using ansst1. 2knockout zebrafish model and a combination of techniques, including Alisin blue cartilage staining, Alizarin red sclerosteum staining, micro-CT scanning, calcium xanthophyll labelling, and expression analysis of key osteogenic genes. The results showed thatsst1. 2deletion did not significantly affect cartilage development or intramembranous ossification of the spine, but significantly increased the bone mass of the zebrafish mutant skull. The development of scales was not affected. Histological analysis and osteogenic gene expression confirmed that the increased bone mass was due to enhanced endochondral ossification. These results suggested that SST signaling regulated bone mass by inhibiting endochondral ossification during zebrafish osteogenesis. The findings provided a new theoretical basis for a deeper understanding of skeletal development in fish and suggest new ideas for establishing more accurate models of skeletal dysplasia diseases, such as bone metabolic disorders.

Key words: somatostatin, bone mass, endochondral ossification, zebrafish, CRISPR/Cas9

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