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GW24-e1281 Alpha-linolenic acid intake protects endothelial function in diabetic rats and the involved mechanisms
  1. Xiangyan Liang1,
  2. Wei Zhang2,
  3. Rong Li3,
  4. Fei Tian1,
  5. Siwang Wang4,
  6. Qiangsun Zheng2,
  7. Haifeng Zhang1
  1. 1Experiment Teaching Center, Fourth Military Medical University, Xi’an, China
  2. 2Department of Cardiology, Tangdu hospital, Fourth Military Medical University, Xi’an, China
  3. 3Department of Geratology, Xijing Hospital, Fourth Military Medical University, Xi’an, China
  4. 4Institute of Pharmaceutical Research, Fourth Military Medical University, Xi’an, China


Objectives Mounting evidence has indicated that the cardiovascular protective effects of dietary alpha-linolenic acid (ALA), but whether ALA may exert an endothelial protective effect against high glucose injury and the underlying mechanisms remain largely unknown.

Methods Streptozocin-induced diabetic rats were randomised into vehicle (0.01% alcohol) or ALA (500 μg/kg/d) for 4 weeks. Human umbilical vein endothelial cells (HUVECs) were exposed to high glucose (28 mmol/L) stimulation for 48 hours.

Results ALA significantly improved concentration-dependent vasorelaxation to ACh in diabetic aortic segments and inhibited endothelial inflammation as evidenced by decreased soluble P-selectin and intercellular adhesion molecule-1 (ICAM-1) in diabetic rats (n = 6-8, P < 0.05). Furthermore, both P-selectin and ICAM-1 expression were significantly increased in high glucose-induced HUVECs, resulting in enhanced neutrophils adhesion to HUVECs compared with normal glucose group (P < 0.01). Treatment with ALA (50 μmol/L) increased Akt phosphorylation, attenuated P-selectin and ICAM-1 expression and thus inhibited neutrophils adhesion in HUVECs exposed to high glucose, all of which were blocked by the PI3K inhibitors LY294002 and wortmannin (P < 0.05).

Conclusions These data indicated that ALA inhibited endothelial inflammation and improved endothelial function in STZ-induced diabetic rats. The anti-adhesive effect of ALA against high glucose injury may partially be mediated by the PI3K/Akt pathway.

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