...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >GLP-1 and Ghrelin Attenuate High Glucose/High Lipid-Induced Apoptosis and Senescence of Human Microvascular Endothelial Cells
【24h】

GLP-1 and Ghrelin Attenuate High Glucose/High Lipid-Induced Apoptosis and Senescence of Human Microvascular Endothelial Cells

机译：GLP-1和Ghrelin减轻高糖/高脂质诱导的人微血管内皮细胞凋亡和衰老

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

>Background/Aims: GLP-1 and ghrelin are common appetite-regulating hormones. Both have multiple functions beyond metabolic regulation. However, the effects of GLP-1 and ghrelin on endothelial biology are not fully understood. Here, we investigate the roles of GLP-1 and ghrelin in microvascular endothelial apoptosis and senescence. Methods: Human microvascular endothelial cells (HMECs) were exposed to high glucose/high lipid (HG/HL) conditions and treated with GLP-1 or ghrelin. Cellular apoptosis, senescence, and mitochondrial function were measured. In addition, the MAPK and Akt signaling pathways were examined. Results: Both GLP-1 and ghrelin treatment decreased the number of TUNEL-positive cells and inhibited caspase-3 and PARP cleavage and mitochondrial dysfunction in HG/HL-exposed HMECs. GLP-1, but not ghrelin decreased the number of ?2-galactosidase (?2-gal)-positive cells. Furthermore, GLP-1 and ghrelin inhibited ERK1/2, JNK1/2, and p38 signaling. GLP-1 suppressed Akt signaling, but ghrelin had no effect. Moreover, JNK1/2 and p38 inhibitors, but not ERK1/2 and Akt inhibitors, decreased the number of TUNEL-positive cells. Additionally, only the Akt inhibitor decreased the number of ?2-gal-positive cells. Conclusion: These results demonstrate that GLP-1 and ghrelin inhibit mitochondrial dysfunction under HG/HL conditions, and suppress endothelial apoptosis via inhibiting JNK1/2 and p38 signaling; moreover, GLP-1 alleviates endothelial senescence via inactivating Akt signaling.
机译：> 背景/目的： GLP-1和Ghrelin是常见的食欲调节激素。两者都具有代谢调节以外的多种功能。但是，尚未完全了解GLP-1和Ghrelin对内皮生物学的影响。在这里，我们调查GLP-1和ghrelin在微血管内皮细胞凋亡和衰老中的作用。 方法： 将人微血管内皮细胞（HMEC）暴露于高葡萄糖/高脂质（HG / HL）条件下，并用GLP-1或生长素释放肽处理。测量细胞凋亡，衰老和线粒体功能。另外，检查了MAPK和Akt信号通路。 结果： 在HG / HL暴露的HMEC中，GLP-1和ghrelin均可减少TUNEL阳性细胞的数量，并抑制caspase-3和PARP裂解以及线粒体功能障碍。 GLP-1而非Ghrelin减少了β2-半乳糖苷酶（β2-gal）阳性细胞的数量。此外，GLP-1和Ghrelin抑制ERK1 / 2，JNK1 / 2和p38信号传导。 GLP-1抑制了Akt信号传导，但生长素释放肽没有作用。此外，JNK1 / 2和p38抑制剂可降低TUNEL阳性细胞的数量，而ERK1 / 2和Akt抑制剂则不会。另外，仅Akt抑制剂减少了β2-gal阳性细胞的数量。 结论： 这些结果表明，GLP-1和Ghrelin在HG / HL条件下抑制线粒体功能障碍，并通过抑制JNK1 / 2和p38信号传导抑制内皮细胞凋亡。此外，GLP-1通过灭活Akt信号传导减轻内皮细胞的衰老。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号