Nicotinamide mononucleotide (NMN) protects bEnd.3 cells against H2O2‐induced damage via NAMPT and the NF‐κB p65 signalling pathway,FEBS Open Bio

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Nicotinamide mononucleotide (NMN) protects bEnd.3 cells against H2O2‐induced damage via NAMPT and the NF‐κB p65 signalling pathway
FEBS Open Bio ( IF 2.8 ) Pub Date : 2020-12-19 , DOI: 10.1002/2211-5463.13067
Xiujun Deng ₁ , Xinghuan Liang ₂ , Haiyan Yang ₂ , Zhenxing Huang ₂ , Xuemei Huang ₂ , Chunfeng Liang ₃ , Yaqi Kuang ₂ , Yingfen Qin ₂ , Faquan Lin ₁ , Zuojie Luo ₂

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An increasing number of studies have shown that nicotinamide mononucleotide (NMN) can inhibit not only ageing but also oxidative stress and inflammatory reactions by improving energy metabolism. However, the role of NMN in regulating the anti‐apoptotic, antioxidative stress and inflammatory responses of brain microvascular endothelial cells is still unknown. Therefore, here we studied the effects of NMN on H₂O₂‐induced oxidative damage of bEnd.3 cells. In this study, we found that NMN could inhibit the NF‐κBp65 inflammatory signalling pathway and increase the expression of the enzymes NAMPT, VEGF and eNOS, alleviating H₂O₂‐induced apoptosis in bEnd.3 cells. Taken together, these results suggest that NMN reduces H₂O₂‐induced oxidative stress and apoptosis and improves cell functions by inhibiting the NF‐κBp65 inflammatory pathway and increasing NAMPT expression.

中文翻译：

烟酰胺单核苷酸 (NMN) 通过 NAMPT 和 NF-κB p65 信号通路保护 bEnd.3 细胞免受 H2O2 诱导的损伤

越来越多的研究表明，烟酰胺单核苷酸（NMN）不仅可以通过改善能量代谢来抑制衰老，还可以抑制氧化应激和炎症反应。然而，NMN在调节脑微血管内皮细胞抗凋亡、抗氧化应激和炎症反应中的作用仍不清楚。因此，我们在此研究了NMN对H ₂ O ₂诱导的bEnd.3细胞氧化损伤的影响。在本研究中，我们发现 NMN 可以抑制 NF-κBp65 炎症信号通路，增加酶 NAMPT、VEGF 和 eNOS 的表达，减轻 H ₂ O ₂诱导的 bEnd.3 细胞凋亡。总之，这些结果表明 NMN 降低了 H ₂O ₂诱导的氧化应激和细胞凋亡，并通过抑制 NF-κBp65 炎症通路和增加 NAMPT 表达来改善细胞功能。

更新日期：2020-12-19

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