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Hydrogen-rich water prevents lipid deposition in the descending aorta in a rat periodontitis model


Hydrogen Water Studies

AtherosclerosisGingivitis

Hydrogen-rich water prevents lipid deposition in the descending aorta in a rat periodontitis model

by Daisuke Ekuni, Koichiro Irie, Manabu Morita, Takaaki Tomofuji, Naofumi Tamaki, Kenta Kasuyama, Azusa Kojima, Shinsuke Mizutani, Tatsuji Azume, Yasumasa Endo

Abstract:

Objective: Periodontitis has been causally linked to atherosclerosis, which is mediated by the oxidative stress. As hydrogen-rich water (HW) scavenges reactive oxygen species (ROS), we hypothesized that HW could prevent lipid deposition induced by periodontitis in the aorta. The aim of this study was to investigate the effects of HW on the initiation of atherosclerosis in a rat periodontitis model. Design: Eighteen 8-wk-old male Wistar rats were divided into three groups of six rats; the periodontitis group, periodontitis+HW group and the no treatment (control) group. In the periodontitis and periodontitis+HW groups, periodontitis was induced using a ligature for 4 wk, while the periodontitis+HW group was given water containing 800-1000 μg/L hydrogen during the 4-wk experimental period. Results: In the periodontitis group, lipid deposition in the descending aorta was observed. The periodontitis group also showed significant higher serum levels for ROS and oxidised low-density lipoprotein-cholesterol (ox-LDL) (1.7 and 1.4 times, respectively), and higher aortic expression levels of nitrotyrosine and hexanoyl-lysine (HEL) (7.9 and 16.0 times, respectively), as compared to the control group (p<0.05). In the periodontitis+HW group, lipid deposition was lower. Lower serum levels of ROS and ox-LDL (0.46 and 0.82 times, respectively) and lower aortic levels of nitrotyrosine and HEL (0.27 and 0.19 times, respectively) were observed in the periodontitis+HW group than in the periodontitis group (p<0.05). Conclusions: HW intake may prevent lipid deposition in the rat aorta induced by periodontitis by decreasing serum ox-LDL levels and aortic oxidative stress.

Read more:

https://doi.org/10.1016/j.archoralbio.2012.04.013

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Sam Soliman

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