胸腺素β4通过增加一氧化氮合成影响晚期内皮祖细胞的衰老
hymosin β4 ameliorates senescence of late endothelial progenitor cell through augmentation of nitric oxide production
我们既往的研究表明，胸腺素β4（Tβ4）可以通过PI3K-Akt-eNOS信号转导通路抑制早期（EPC）的衰老，但不明确Tβ4是否对晚期EPC有类似作用、是否通过其信号通路下游的内皮型一氧化氮合酶－一氧化氮（eNOS-NO）系统增加NO的合成进而抑制EPC衰老。在本实验中，我们发现Tβ4呈浓度梯度依赖性地减少了晚期EPC的衰老。而且Tβ4可以上调eNOS的磷酸化并增加NO的合成，且其对晚期EPC的抗衰老作用可以被eNOS的小干扰RNA（siRNA）所逆转。此外，一定浓度的NO的供体硝普钠也可以类似地抑制晚期EPC的衰老。因此，Tβ4通过激活eNOS-NO和增加NO的合成发挥对晚期EPC的抗衰老作用。 ?????
Our previous study showed that thymosin β4 (Tβ4) inhibited senescence of early endothelial progenitor cell (EPC) through PI3K-Akt-eNOS signaling pathway. However, whether Tβ4 has similar anti-senescent effect on late EPC, reduces senescence of EPC via activation of downstream eNOS-NO system and augmentation the production of nitric oxide remains unclear. In this study, we showed that Tβ4 inhibited late EPC senescence in a concentration-dependent manner, which was similar to early EPC in our previous investigation. Besides, Tβ4 upregulated the phosphorylation of eNOS and augmented the production of nitric oxide. The anti-senescence effect of Tβ4 on EPC could be abolished by eNOS siRNA. Interestingly, sodium nitroprusside, a nitric oxide donnor could reduce senescence of EPC similarly. In conclusion, Tβ4 inhibited senescence of EPC via activation of eNOS-NO system and increase of production of nitric oxide.
宋佳乐、赵炎波、傅国胜、邱福宇
基础医学生理学生物化学
胸腺素 β4内皮祖细胞细胞衰老一氧化氮
hymosin β4endothelial progenitor cellcell senescencenitric oxide
宋佳乐,赵炎波,傅国胜,邱福宇.胸腺素β4通过增加一氧化氮合成影响晚期内皮祖细胞的衰老[EB/OL].(2013-12-24)[2025-08-04].http://www.paper.edu.cn/releasepaper/content/201312-736.点此复制
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