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梓醇通过激活 HIF-1α/VEGF 信号通路调节内皮细胞凋亡和增殖。

Catalpol regulates apoptosis and proliferation of endothelial cell via activating HIF-1α/VEGF signaling pathway.

机构信息

Department of Orthopedics, Suqian First Hospital, Suqian, China.

Suqian First Hospital, No. 120 Suzhi Road, Suqian, Jiangsu, China.

出版信息

Sci Rep. 2024 Nov 16;14(1):28327. doi: 10.1038/s41598-024-78126-7.

DOI:10.1038/s41598-024-78126-7
PMID:39550364
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11569138/
Abstract

Burn injuries, especially severe ones, causes microcirculation disorders in local wounds and distant tissues, leading to ischemia and hypoxia of body tissues and organs. The key to prevent and treat complications and improve prognosis after burns is to improve the state of ischemia and hypoxia of tissue and restore the blood supply of organs. Catalpol is an iridoid glycoside compound isolated from Rehmannia radix, which has been widely reported to have various of functions, including antioxidative stress, anti-inflammation, anti-apoptosis, and neuroprotection. However, the pharmacologic action and underlying mechanism of Catalpol in angiogenesis after burn injury remains unclear. The study investigated whether Catalpol regulates apoptosis and proliferation following vascular injury induced by burns using an in vitro model of oxygen-glucose deprivation (OGD) with a human umbilical vein endothelial (HUVE) cell line. The results showed that treatment with Catalpol reduces the level of apoptosis and promotes proliferation of endothelial cell. Mechanistically, Catalpol increases the expression of vascular endothelial growth factor (VEGF) by activating Hypoxia-inducible factor-1α (Hif-1α), resulting in increased expression of related downstream effector molecules. The current study suggested that Catalpol is a promising compound for endothelial protection in burns. It may be an efficient Hif-1α activator for endothelial cell deprived of oxygen and glucose.

摘要

烧伤,尤其是严重的烧伤,会导致局部伤口和远处组织的微循环障碍,导致组织和器官的缺血缺氧。预防和治疗烧伤后并发症、改善预后的关键是改善组织的缺血缺氧状态,恢复器官的血液供应。梓醇是从地黄中分离得到的环烯醚萜苷类化合物,已广泛报道具有多种功能,包括抗氧化应激、抗炎、抗细胞凋亡和神经保护。然而,梓醇在烧伤后血管生成中的药理作用和作用机制尚不清楚。本研究利用人脐静脉内皮(HUVE)细胞系的体外氧葡萄糖剥夺(OGD)模型,探讨梓醇是否通过调节烧伤诱导的血管损伤后的细胞凋亡和增殖来发挥作用。结果表明,梓醇处理可降低内皮细胞凋亡水平,促进其增殖。机制上,梓醇通过激活低氧诱导因子-1α(Hif-1α)增加血管内皮生长因子(VEGF)的表达,从而增加相关下游效应分子的表达。本研究提示梓醇可能是一种有前途的烧伤内皮保护化合物。它可能是一种有效的缺氧和葡萄糖剥夺内皮细胞 Hif-1α激活剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/8a3cfab2f69b/41598_2024_78126_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/e9fa459d94a5/41598_2024_78126_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/d1f8d9056a6e/41598_2024_78126_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/c31b6d0b8ef7/41598_2024_78126_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/0a172464e3b4/41598_2024_78126_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/8a3cfab2f69b/41598_2024_78126_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/e9fa459d94a5/41598_2024_78126_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/d1f8d9056a6e/41598_2024_78126_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/c31b6d0b8ef7/41598_2024_78126_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/0a172464e3b4/41598_2024_78126_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7719/11569138/8a3cfab2f69b/41598_2024_78126_Fig5_HTML.jpg

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