Chen Wenting, Huang Caoxin, Yang Chen, Ge Xilin, Huang Wenfang, Li Xuejun, Yang Shuyu, Liu Suhuan
Xiamen Diabetes Institute, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Medical College of Xiamen University, Xiamen 361000, China.
Evid Based Complement Alternat Med. 2018 Jul 10;2018:5421023. doi: 10.1155/2018/5421023. eCollection 2018.
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 (CoCl) induced damage, including cell viability, proliferation, and tube formation. Furthermore, DSD-CS restored the activity of PI3K/Akt/eNOS signaling inhibited by CoCl 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.
当归四逆汤（DSD）是一种传统的中药汤剂，被广泛应用且显示出在改善缺血相关症状方面有效。然而，DSD在缺血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关键组成部分，对缺氧损伤高度敏感。在此，我们以胰岛内皮细胞系MST1细胞为模型，研究了DSD对缺氧刺激的内皮细胞损伤的影响及其潜在机制。我们发现，从经DSD处理的大鼠中收集的含DSD血清（DSD-CS）能够有效保护MST1细胞的存活和增殖免受氯化钴（CoCl）诱导的损伤，包括细胞活力、增殖和管形成。此外，DSD-CS恢复了MST1细胞中被CoCl抑制的PI3K/Akt/eNOS信号通路的活性。DSD-CS的保护作用可被特异性PI3K/Akt/eNOS抑制剂LY294002阻断，这表明DSD-CS对MST1细胞在缺氧状态下存活的保护作用是通过PI3K/Akt/eNOS途径介导的。总之，DSD处理通过PI3K/Akt/eNOS途径保护MST1细胞免受缺氧损伤，表明其在保护微血管内皮细胞中的作用。
