Safi, Sher Zaman and Shah, Humaira and Qvist, Rajes and Bindal, Priyadarshni and Mansor, Marzida and Ong, Gracie Siok Yan and Ismail, Ikram Shah (2018) Beta Adrenergic Receptors Stimulation Attenuates Phosphorylation of NF-κB and IκBα in Hyperglycemic Endothelial Cells. Cellular Physiology and Biochemistry, 51 (3). pp. 1429-1436. ISSN 1015-8987, DOI https://doi.org/10.1159/000495591.
Full text not available from this repository.Abstract
Background/Aims: NF-κB induces transcription of a number of genes, associated with inflammation and apoptosis. In this study, we have investigated the effect of β-adrenergic receptor stimulation on NF-κB and IκBα in HUVECs. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured in high and low glucose concentrations. All HUVECs were treated with different concentrations of isoproterenol and propranolol for different time periods. The analytical procedures consisted of Western Blot, ELISA, DCFH-DA and TUNEL assays. Results: Isoproterenol (agonist of a beta-adrenergic receptor) significantly reduced phosphorylation at Ser-536 of NF-κB; and Ser-32 and Ser-36 of IκBα in hyperglycemic HUVECs. Isoproterenol also significantly reduced apoptosis and ROS generation. No effect of IκBα was observed on Tyr-42 phosphorylation. The effect of isoproterenol was reversed by the antagonist propranolol. We also checked if NF-κB inhibitor MG132 causes any change at the level of apoptosis. However, we observed an almost similar effect. Conclusion: Given data demonstrates that beta-adrenergic receptors stimulation has a protective effect on HUVECs that might be occuring via NF-κβ and IκBα pathway.
Item Type: | Article |
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Funders: | UNSPECIFIED |
Uncontrolled Keywords: | Beta Adrenergic receptors; Hyperglycemia-induced inflammation; Apoptosis; NF-κB; HUVECs |
Subjects: | R Medicine |
Divisions: | Faculty of Medicine |
Depositing User: | Ms. Juhaida Abd Rahim |
Date Deposited: | 08 Apr 2019 04:30 |
Last Modified: | 08 Apr 2019 04:30 |
URI: | http://eprints.um.edu.my/id/eprint/20828 |
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