TY - JOUR
T1 - Inhibition of retinal ischemia–reperfusion injury in rats by inhalation of low-concentration hydrogen gas
AU - Otsuka, Mitsuya
AU - Arai, Kenichi
AU - Yoshida, Toshiko
AU - Hayashi, Atsushi
N1 - Publisher Copyright:
© The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. corrected publication 2023.
PY - 2024/3
Y1 - 2024/3
N2 - 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.
AB - 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.
KW - Cytokine
KW - Hydrogen gas
KW - Inhalation
KW - Ischemia–reperfusion injury
KW - Retina
UR - http://www.scopus.com/inward/record.url?scp=85174411866&partnerID=8YFLogxK
U2 - 10.1007/s00417-023-06262-3
DO - 10.1007/s00417-023-06262-3
M3 - 学術論文
C2 - 37851131
AN - SCOPUS:85174411866
SN - 0721-832X
VL - 262
SP - 823
EP - 833
JO - Graefe's Archive for Clinical and Experimental Ophthalmology
JF - Graefe's Archive for Clinical and Experimental Ophthalmology
IS - 3
ER -