Inhibition of retinal ischemia–reperfusion injury in rats by inhalation of low-concentration hydrogen gas

Mitsuya Otsuka, Kenichi Arai, Toshiko Yoshida, Atsushi Hayashi*

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

2 被引用数 (Scopus)

抄録

Purpose: To investigate the inhibitory effect of hydrogen gas inhalation on retinal ischemia reperfusion (I/R) injury using a rat model. Methods: Six-week-old male Sprague–Dawley rats were used. A 27G needle connected by a tube to a saline bottle placed 200 cm above the eye was inserted into the anterior eye chamber to create a rat retinal I/R model. In the ischemia-plus-hydrogen-gas group (H2(+) group), the ischemia time was set to 90 min, and 1.8% hydrogen was added to the air delivered by the anesthesia mask simultaneously with the start of ischemia. In the non-hydrogen-treatment ischemia group (H2(−) group), I/R injury was created similarly, but only air was inhaled. ERGs were measured; after removal of the eyes, the retina was examined for histological, immunostaining, and molecular biological analyses. Results: The mean thickness of the inner retinal layer in the H2(+) group was 107.2 ± 16.0 μm (n = 5), significantly greater than that in the H2(−) group (60.8 ± 6.7 μm). Immunostaining for Iba1 in the H2(−) group showed increased numbers of microglia and microglial infiltration into the subretinal space, while there was no increase in microglia in the H2(+) group. B-wave amplitudes in the H2(+) group were significantly higher than in the H2(−) group. In the membrane antibody array, levels of interleukin-6, monocyte chemotactic protein 1, and tumor necrosis factor alpha were significantly lower in the H2(+) group than in the H2(−) group. Conclusion: Inhalation of 1.8% hydrogen gas inhibited the induction of inflammation, morphological/structural changes, and glial cell increase caused by retinal I/R injury.

本文言語英語
ページ(範囲)823-833
ページ数11
ジャーナルGraefe's Archive for Clinical and Experimental Ophthalmology
262
3
DOI
出版ステータス出版済み - 2024/03

ASJC Scopus 主題領域

  • 眼科学
  • 感覚系
  • 細胞および分子神経科学

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