胃饥饿素对低氧相关心脏血管生成的影响：miR-210 信号通路的参与。
Effect of ghrelin on hypoxia-related cardiac angiogenesis: involvement of miR-210 signalling pathway.
机构信息
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
出版信息
Arch Physiol Biochem. 2022 Feb;128(1):270-275. doi: 10.1080/13813455.2019.1675712. Epub 2019 Oct 9.
OBJECTIVE
Hypoxia is the main stimulus for angiogenesis. Hypoxia-inducible factor (HIF)-1α, vascular endothelial growth factor (VEGF), and miR-210 are involved in the hypoxia-induced angiogenesis. This study examined the effects of hypoxia and/or ghrelin on miR-210, HIF-1α, and VEGF levels in the heart of rats.
METHODS
Wistar rats were randomly divided into 4 groups ( = 6): control; ghrelin, received daily intraperitoneal injections of ghrelin; hypoxia, was exposed to hypoxic condition; hypoxia + ghrelin, was exposed to hypoxic condition and received intraperitoneal injections of ghrelin, for 2 weeks. Myocardial angiogenesis, the expression level of miR-210, and protein levels of HIF-1α and VEGF were assayed in the heart samples.
RESULTS
Hypoxia increased myocardial angiogenesis and cardiac levels of miR-210, HIF-1α, and VEGF. However, ghrelin inhibited these hypoxia-induced changes. Interestingly, ghrelin had no significant effect on miR-210, HIF-1α, and VEGF levels in normoxic condition.
CONCLUSION
Ghrelin may be useful as an anti-angiogenic factor.
目的
缺氧是血管生成的主要刺激因素。缺氧诱导因子（HIF）-1α、血管内皮生长因子（VEGF）和 miR-210 参与了缺氧诱导的血管生成。本研究探讨了缺氧和/或胃饥饿素对大鼠心脏中 miR-210、HIF-1α 和 VEGF 水平的影响。
方法
将 Wistar 大鼠随机分为 4 组（每组 6 只）：对照组；给予胃饥饿素的胃饥饿素组，每天接受腹腔注射胃饥饿素；缺氧组，暴露于缺氧环境；缺氧+胃饥饿素组，暴露于缺氧环境并接受腹腔注射胃饥饿素，持续 2 周。检测心脏样本中的心肌血管生成、miR-210 的表达水平以及 HIF-1α 和 VEGF 的蛋白水平。
结果
缺氧增加了心肌血管生成和心脏中 miR-210、HIF-1α 和 VEGF 的水平。然而，胃饥饿素抑制了这些缺氧诱导的变化。有趣的是，胃饥饿素在常氧条件下对 miR-210、HIF-1α 和 VEGF 水平没有显著影响。
结论
胃饥饿素可能作为一种抗血管生成因子具有应用价值。
Zotero 插件