Scholarlink

Background <p>Stroke is a cerebrovascular disease that is the main cause of death and disability worldwide. Hypoxia is a major factor that causes neuronal damage and even cellular death. However, the mechanism and therapeutic drugs for hypoxia are not completely understood.</p> Methods <p>In this study, PC12 cells (a rat adrenal pheochromocytoma cell line) were exposed to Cobalt chloride (CoCl<sub>2</sub>) to induce hypoxia. Using this cell model, the impacts of hypoxia on cell viability, proliferation, reactive oxygen species (ROS), and the levels of lysine β-hydroxybutyrylation (Kbhb) and the inflammatory signaling factor P65 were examined. In addition, we explored the ability of resveratrol (RES) to alleviate CoCl<sub>2</sub>-induced hypoxia damage.</p> Results <p>RES attenuated CoCl<sub>2</sub>-induced decreases of cell viability and cell proliferation and increase of ROS production in PC12 cells. CoCl<sub>2</sub> downregulated Kbhb in PC12 cells, but RES alleviated this effect. In addition, upregulated Kbhb by 3-hydroxybutyric acid sodium could partially recover the CoCl<sub>2</sub>-induced hypoxia damage to PC12 cells, including cell viability, cell proliferation, oxidative stress, and the protein level of the inflammatory signaling factor P65.</p> Conclusion <p>Our results indicate that RES protects against CoCl<sub>2</sub>-induced hypoxia damage in PC12 cells by modulating Kbhb, a novel post-translational modification.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Resveratrol attenuates the CoCl2-induced hypoxia damage by regulation of lysine β-hydroxybutyrylation in PC12 cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年4月10日

查看全文
  • Yamei Wang,
  • Jian Zhao,
  • Liang Sun,
  • Dingding Xu,
  • Xiaoming Wei,
  • Jia Li,
  • Zihan Mo,
  • Nian Xia,
  • Junge Zhou,
  • Yuan Yao,
  • Qiao Hu,
  • Qingqing Zhou

摘要

Background

Stroke is a cerebrovascular disease that is the main cause of death and disability worldwide. Hypoxia is a major factor that causes neuronal damage and even cellular death. However, the mechanism and therapeutic drugs for hypoxia are not completely understood.

Methods

In this study, PC12 cells (a rat adrenal pheochromocytoma cell line) were exposed to Cobalt chloride (CoCl2) to induce hypoxia. Using this cell model, the impacts of hypoxia on cell viability, proliferation, reactive oxygen species (ROS), and the levels of lysine β-hydroxybutyrylation (Kbhb) and the inflammatory signaling factor P65 were examined. In addition, we explored the ability of resveratrol (RES) to alleviate CoCl2-induced hypoxia damage.

Results

RES attenuated CoCl2-induced decreases of cell viability and cell proliferation and increase of ROS production in PC12 cells. CoCl2 downregulated Kbhb in PC12 cells, but RES alleviated this effect. In addition, upregulated Kbhb by 3-hydroxybutyric acid sodium could partially recover the CoCl2-induced hypoxia damage to PC12 cells, including cell viability, cell proliferation, oxidative stress, and the protein level of the inflammatory signaling factor P65.

Conclusion

Our results indicate that RES protects against CoCl2-induced hypoxia damage in PC12 cells by modulating Kbhb, a novel post-translational modification.