α-Linolenic acid attenuates high glucose-induced apoptosis in cultured human umbilical vein endothelial cells via PI3K/Akt/eNOS pathway
| Autor: | Si-wang Wang, Lun Bu, Rui Wang, Shu-fang Han, Heng Ma, Wei Zhang, Guo-liang Jia |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Umbilical Veins
medicine.medical_specialty Nitric Oxide Synthase Type III Endothelium Endocrinology Diabetes and Metabolism Apoptosis Umbilical vein Nitric oxide Phosphatidylinositol 3-Kinases chemistry.chemical_compound Enos Internal medicine In Situ Nick-End Labeling medicine Humans Phosphorylation Protein kinase B Cells Cultured Nutrition and Dietetics Dose-Response Relationship Drug biology Endothelial Cells alpha-Linolenic Acid Flow Cytometry biology.organism_classification Oncogene Protein v-akt Endothelial stem cell Nitric oxide synthase Glucose medicine.anatomical_structure Endocrinology chemistry biology.protein Human umbilical vein endothelial cell |
| Zdroj: | Nutrition. 23:762-770 |
| ISSN: | 0899-9007 |
| DOI: | 10.1016/j.nut.2007.07.003 |
| Popis: | Objective High glucose-induced apoptosis in vascular endothelial cells contributes to the acceleration of atherosclerosis associated with diabetes. We hypothesized that α-linolenic acid (ALA) might attenuate high glucose-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs). Methods HUVECs were cultured at 5.5 and 33 mmol/L for 72 h. ALA with different concentrations was added with defatted bovine serum albumin as a carrier for 18 h before incubation with high glucose. Results Exposure of HUVECs to high glucose media for 72 h significantly increased the number of apoptotic cells compared with normal glucose control, as evaluated by flow cytometry and terminal deoxyuridine triphosphate nick end labeling assay. Pretreatment with low concentrations of ALA (10, 50, and 100 μmol/L) significantly attenuated high glucose-induced apoptosis of HUVECs, but increasing ALA to 200 μmol/L exerted the opposite effect. Furthermore, high glucose reduced phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production, whereas ALA treatment attenuated the reduction caused by high glucose. Pretreatment with phosphatidylinositol 3’ -kinase kinase inhibitor LY294002 and eNOS inhibitor N G -nitro-arginine methyl esyer eliminated ALA’ antiapoptotic effect. Conclusion ALA exerts an antiapoptotic effect by the phosphatidylinositol 3’-kinase/Akt/eNOS pathway in HUVECs exposed to high glucose and thus may represent a candidate therapeutic agent for diabetic cardiovascular complications. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect