Open AccessMalaysian Tualang Honey Inhibits Hydrogen Peroxide-Induced Endothelial Hyperpermeability
Author(s) -
Kogilavanee Devasvaran,
Jun Jie Tan,
Chin Theng Ng,
Lai Yen Fong,
Yoke Keong Yong
Publication year - 2019
Publication title -
oxidative medicine and cellular longevity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.494
H-Index - 93
eISSN - 1942-0900
pISSN - 1942-0994
DOI - 10.1155/2019/1202676
Subject(s) - oxidative stress , umbilical vein , pharmacology , chemistry , in vivo , evans blue , vascular permeability , hydrogen peroxide , in vitro , biochemistry , biology , endocrinology , microbiology and biotechnology
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- (H 2 O 2 -) 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 H 2 O 2 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 H 2 O 2 (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 H 2 O 2 . These results suggested that TH could inhibit H 2 O 2 -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.