Inhibitory effects of crocetin on high glucose-induced apoptosis in cultured human umbilical vein endothelial cells and its mechanism.

Archives of Pharmacal Research
Lingdong Meng, Lianqun Cui

Abstract

Dysfunction of endothelial cell is considered as a major cause of vascular complications in diabetes. Crocetin has been shown to have strong antioxidant activities. In present study, we tested whether crocetin inhibited high glucose-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs) and to explore its possible mechanism. Exposure to high glucose (33 mM) for 72h induced a pronounced increase in apoptosis compared with normal glucose (5.5 mM), as evaluated by cell chromatin staining with Hoechst 33,258 and cell death detection ELISA. High glucose attenuated activation of Akt and endothelial nitric oxide synthase (eNOS). Crocetin (0.1 microM, 1.0 microM) prevented high glucose-induced apoptosis, which correlates with the increase of activation of p-Akt, following the up-regulation of eNOS and NO production. Pretreatment with phosphatidylinositol 3' kinase (Pl3K) inhibitor LY294002 or eNOS inhibitor NG-nitro-arginine methyl ester (LN or L-NAME) inhibited crocetin effect on p-Akt or eNOS, respectively. For the first time, results of our study suggest that crocetin inhibits high glucose-induced apoptosis, at least partly, via Pl3K/Akt/eNOS pathway in HUVECs and crocetin may exert a beneficial effect in prev...Continue Reading

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Citations

Nov 30, 2012·Apoptosis : an International Journal on Programmed Cell Death·Radhika KapoorPoonam Kakkar
Sep 11, 2010·Critical Reviews in Food Science and Nutrition·S Zahra Bathaie, S Zeinab Mousavi
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Aug 5, 2017·Diabetes & Vascular Disease Research : Official Journal of the International Society of Diabetes and Vascular Disease·Wei ChenHongwei Lu

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AKT Pathway

This feed focuses on the AKT serine/threonine kinase, which is an important signaling pathway involved in processes such as glucose metabolism and cell survival.

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Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

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