DL-3-n-butylphthalide protects endothelial cells against advanced glycation end product-induced injury by attenuating oxidative stress and inflammation responses
| Autor: | Zhi‑Ting Chen, Chun Hui Che, Chang Yun Liu, Sheng‑Gen Chen, Jie You, Zhang-Yu Zou, Han‑Bin Lin, Hua Pin Huang, Zhen‑Hua Zhao, Xiao‑Fan Wei, Yuan‑Xiao Li, Xiao‑Min Wu |
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| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cancer Research Inflammation Pharmacology Biology medicine.disease_cause Umbilical vein Proinflammatory cytokine 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Immunology and Microbiology (miscellaneous) Glycation medicine Endothelial dysfunction Monocyte General Medicine Articles medicine.disease 030104 developmental biology medicine.anatomical_structure chemistry Cancer research Advanced glycation end-product medicine.symptom 030217 neurology & neurosurgery Oxidative stress |
| Popis: | Endothelial dysfunction, regarded as a key step in the pathophysiological course of diabetic vascular complications, is initiated and deteriorated by advanced glycation end products (AGEs). DL-3-n-butylphthalide (DL-NBP) has been proven to have protective effects on neurons and vascular endothelial cells against ischemic and anoxic damage. The aim of the present study was to investigate whether NBP is able to attenuate AGE-induced endothelial dysfunction in vitro, and also elucidate the possible underlying mechanism. An injury model of human umbilical vein endothelial cells (HUVECs) induced by AGEs (200 µg/ml) was established. The results demonstrated that pretreatment with NBP (1-100 µM) significantly increased HUVEC viability and inhibited the apoptosis induced by AGEs. In addition, AGEs stimulated the expression levels of the receptor for AGEs protein and the downstream protein nuclear factor-κB in HUVECs, which were inhibited by pretreatment with NBP. Furthermore, it significantly reduced reactive oxygen species generation and the level of the inflammatory cytokines, intercellular cell adhesion molecule-1 and monocyte chemotactic protein-1, in HUVECs mediated by AGEs. The current findings indicated that NBP attenuated AGE-induced endothelial dysfunction by ameliorating inflammation and oxidative stress responses. |
| Databáze: | OpenAIRE |
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