Malaysian Tualang Honey Inhibits Hydrogen Peroxide-Induced Endothelial Hyperpermeability. (18th August 2019)

• Record Type: Journal Article
• Authors: Devasvaran, Kogilavanee; Tan, Jun Jie; Ng, Chin Theng; Fong, Lai Yen; Yong, Yoke Keong
• Other Names: Carrizzo Albino Guest Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2019(2019)
• Publication Date: 2019-08-18
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2019/1202676
• Languages: English
• ISSNs: 1942-0900

Abstract

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- (H2 O2 -) 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 H2 O2 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 H2 O2 (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 H2 O2 . These results suggested that TH could inhibit H2 O2 -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.