Abstract
Malaysian Tualang honey (TH) is a known therapeutic honey extracted from the honeycombs of the Tualang tree (Koompassia excelsa) and has been reported for its antioxidant, anti-inflammatory, antiproliferative, and wound healing properties. However, the possible vascular protective effect of TH against oxidative stress remains unclear. In this study, the effects of TH on hydrogen peroxide- (H2O2-) elicited vascular hyperpermeability in human umbilical vein endothelial cells (HUVECs) and Balb/c mice were evaluated. Our data showed that TH concentrations ranging from 0.01% to 1.00% showed no cytotoxic effect to HUVECs. Induction with 0.5 mM H2O2 was found to increase HUVEC permeability, but the effect was significantly reversed attenuated by TH (p < 0.05), of which the permeability with the highest inhibition peaked at 0.1%. In Balb/c mice, TH (0.5 g/kg-1.5 g/kg) significantly (p < 0.05) reduced H2O2 (0.3%)-induced albumin-bound Evans blue leak, in a dose-dependent manner. Immunofluorescence staining confirmed that TH reduced actin stress fiber formation while increasing cortical actin formation and colocalization of caveolin-1 and β-catenin in HUVECs. Signaling studies showed that HUVECs pretreated with TH significantly (p < 0.05) decreased intracellular calcium release, while sustaining the level of cAMP when challenged with H2O2. These results suggested that TH could inhibit H2O2-induced vascular hyperpermeability in vitro and in vivo by suppression of adherence junction protein redistribution via calcium and cAMP, which could have a therapeutic potential for diseases related to the increase of both oxidant and vascular permeability.
Highlights
Vascular diseases are among the leading causes of death worldwide, as they are linked to major illnesses such as atherosclerosis, hypertension, and rheumatoid arthritis [1]
To study the cytotoxicity of Tualang honey (TH), human umbilical vein endothelial cells (HUVECs) were treated with 0.001%, 0.01%, 0.10%, 1.00%, 2.00%, 4.00%, 6.00%, 8.00%, and 10.00%
At 2.00% of TH, HUVEC viability was significantly reduced to 78.01% as compared to the untreated control (p < 0 05), and the calculated LD50 of TH was 3.7%
Summary
Vascular diseases are among the leading causes of death worldwide, as they are linked to major illnesses such as atherosclerosis, hypertension, and rheumatoid arthritis [1]. These diseases occur upon an alteration in the homeostatic function in the vascular system. Vascular homeostasis is regulated by the endothelial cell monolayer integrity, which is responsible for the impermeable nature of blood vessels. Changes in endothelial integrity compromise vascular permeability, a physiological response commonly seen in inflammation and angiogenesis [1]. Oxidative stress is defined as an imbalance between oxidants and antioxidants in cells due to overproduction of reactive oxygen species (ROS). ROS plays a dynamic role in modulating several signaling pathways, related to cell differentiation and growth [3]
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