通过抗氧化对球囊扩张引起的血管损伤具有保护作用

本研究来自第三军医大学，该大学目前已经发表2篇氢气生物学效应研究，几个月前整形外科曾发表在BBRC上关于氢气治疗糖尿病皮肤炎症方面的细胞学研究，现在的研究是氢气在介入治疗中重要的血管损伤的保护作用，文章发表在国际知名杂志《动脉硬化》上。该学校去年曾经获得2项国家自然科学基金是关于氢气生物学研究的，目前已经开展大量氢气对各类损伤治疗的深入研究，相信不久将会有更多高质量的研究论文见报。

血管内膜增生及其由此所造成的管腔狭窄乃至阻塞，一直是困扰血管外科的一大难题。针对内膜增生发病机制的各个环节，人们采取了一系列的治疗方案，以期达到阻断内膜增生的发生发展，进一步提高血管手术后远期通畅率的目的。

近年来，经皮腔内血管成形术、冠脉气囊成形术等血管手术的应用十分广泛。但是，由内膜增生导致术后血管再栓塞的存在，一直是困扰血管外科的难题，它使手术后远期通畅率难以提高，导致复发。

由于氧化损伤是血管内膜增生的重要原因，氢气作为一种抗氧化物质，在许多氧化损伤疾病中证明有显著的效果，本研究试图证明氢气在球囊扩张引起的血管内膜增生中的作用。通过观察炎症反应和氧化应激等指标，结果证明氢气在预防血管内膜增生中具有显著作用。氢气在血管介入等相关领域具有潜在的临床应用前景。

Atherosclerosis
In Press, Accepted Manuscript - Note to users

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Hydrogen -rich saline prevents neointima formation after carotid balloon injury by suppressing ROS and the TNF-α/NF-κB pathway

Zhe-xue Qin^a, 1, Pan Yu^b, 1, De-hui Qian^a, Ming-bao Song^a, Wei Li^a, Hang Wang^a, Jie Liu^a, Hu Tan^a, Qiang Wang^a, Xue-jun Sun^c, Hong Jiang^a, Jin-kun Zhu^a, Wei Lu^a, Lan Huang^{a,  ,  ,} 

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Received 27 April 2011; revised 4 November 2011; Accepted 4 November 2011. Available online 11 November 2011.

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.