Danggui Sini Decoction Protected Islet Endothelial Cell Survival from Hypoxic Damage via PI3K/Akt/eNOS Pathway.

Danggui Sini Decoction Protected Islet Endothelial Cell Survival from Hypoxic Damage via PI3K/Akt/eNOS Pathway.
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当归四逆汤通过 PI3K/Akt/eNOS 通路保护胰岛内皮细胞免受缺氧损伤

DOI:
10.1155/2018/5421023
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发表时间:
2018
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
通讯作者:
Liu S
Liu S
中科院分区:
其他
文献类型:
--
作者:
Chen W;Huang C;Yang C;Ge X;Huang W;Li X;Yang S;Liu S

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当归四逆汤是一种应用广泛的中药汤剂,具有明显的改善缺血相关症状的作用。然而,DSD在缺血性损伤中的作用机制仍有待充分阐明。胰岛内皮细胞是胰岛微血管的重要组成部分,对缺氧损伤具有高度敏感性。本文以胰岛内皮细胞株MST 1为模型,研究了DSD对缺氧诱导的内皮细胞损伤的影响及其机制。我们发现,从DSD处理的大鼠中收集的含DSD血清(DSD-CS)可以有效地保护MST 1的存活和增殖免受氯化钴(CoCl 2)诱导的损伤,包括细胞活力、增殖和管形成。此外,DSD-CS恢复了CoCl 2抑制的MST 1细胞PI 3 K/Akt/eNOS信号通路的活性。DSD-CS的保护作用可被PI 3 K/Akt/eNOS特异性抑制剂LY 294002所阻断,提示DSD-CS通过PI 3 K/Akt/eNOS通路保护MST 1细胞的缺氧存活。总之,DSD处理通过PI 3 K/Akt/eNOS通路保护MST 1免于缺氧损伤,表明其在保护微血管内皮细胞中的作用。
Danggui Sini decoction (DSD) is a traditional Chinese decoction, which is wildly applied and showed to be effective in ameliorating ischemia-related symptoms. However, the mechanisms of DSD action in ischemic damage remain to be fully clarified. Pancreatic islet endothelial cells are pivotal constituent of islet microvasculature, with high vulnerability to hypoxic injuries. Here, using MST1 cell, a pancreatic islet endothelial cell-line, as a model, we investigated the effects of DSD on hypoxia-stimulated endothelial cell lesions and its underlying mechanisms. We found that DSD-Containing Serum (DSD-CS), collected from DSD-treated rats, could efficiently protect MST1 survival and proliferation from Cobalt chloride (CoCl2) induced damage, including cell viability, proliferation, and tube formation. Furthermore, DSD-CS restored the activity of PI3K/Akt/eNOS signaling inhibited by CoCl2 in MST1 cells. The protective effect of DSD-CS could be blocked by the specific PI3K/Akt/eNOS inhibitor LY294002, suggesting that DSD-CS protection of MST1 cell survival from hypoxia was mediated by PI3K/Akt/eNOS pathway. In conclusion, DSD treatment protected MST1 survival from hypoxic injuries via PI3K/Akt/eNOS pathway, indicating its role in protecting microvascular endothelial cells.
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