Hydrogen Therapy Prevents Artery Blockage After Balloon Surgery
- Authors
- Zhe-xue Qin, Pan Yu, De-hui Qian, Ming-bao Song, Hu Tan, Yang Yu, Wei Li, Hang Wang, Jie Liu, Qiang Wang, Xue-jun Sun, Hong Jiang, Jin-kun Zhu, Wei Lu, Lan Huang
- Journal
- Atherosclerosis
- Year
- 2012
- DOI
- 10.1016/j.atherosclerosis.2011.11.002
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Restenosis
- Body System
- Cardiovascular
TL;DR
A hydrogen-rich saline solution can help prevent the thickening of artery walls after balloon injury by reducing harmful oxidative stress and inflammation.
Key Finding
Hydrogen-rich saline significantly reduced abnormal tissue growth after balloon injury to rat arteries by suppressing reactive oxygen species and blocking inflammatory signaling pathways.
Summary
Researchers tested whether hydrogen-rich saline (a solution containing dissolved hydrogen gas) could prevent abnormal tissue growth in rat arteries after balloon injury. They found that hydrogen-rich saline reduced this unwanted tissue growth by decreasing harmful molecules called reactive oxygen species and blocking inflammatory pathways in the artery wall.
Practical Takeaway
This rat study suggests hydrogen may help prevent restenosis (re-narrowing of arteries after angioplasty), but human trials are needed to determine if these results apply to people. The study was conducted only in animals, so it represents early-stage research rather than evidence of benefit in humans.
Abstract
Background: Reactive oxygen species (ROS) play a pivotal role in neointima hyperplasia after balloon injury. Molecular hydrogen has emerged as a novel antioxidant and has been proven effective in treating many diseases. Objectives: We aimed to determine the mechanism by which hydrogen affects neointima formation. Methods: We assessed the influence of a hydrogen-rich saline solution (HRSS) by daily injection in rats. Rats were euthanized to evaluate the neointima. ROS, malondialdehyde (MDA) and superoxide dismutase (SOD) and reduced glutathione (GSH), were detected in the injured artery. Macrophage infiltration and the production of inflammatory factors (i.e., IL-6, TNF-α and NF-κB) were also observed. The in vitro effects of hydrogen on vascular smooth muscle cell (VSMC) proliferation were also measured. Results: HRSS decreased the neointima area significantly. The neointima/media ratio was also reduced by HRSS. There was a decline in the number of PCNA-positive cells in the intima treated with HRSS. Meanwhile, HRSS ameliorated the ROS and MDA levels and increased SOD, reduced GSH levels in the injured carotid. In addition, the levels of inflammatory factors, such as IL-6, TNF-α and NF-κB p65, were attenuated by HRSS. In vitro studies also confirmed the anti-proliferative capability of the hydrogen solution and ROS generation in VSMCs induced by PDGF-BB. Conclusion: HRSS may have a protective role in the prevention of neointima hyperplasia and restenosis after angioplasty. HRSS may partially exert its role by neutralizing the local ROS and suppressing the TNF-α/NF-κB pathway.