CLC number: Q74; R459.9
On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
Crosschecked: 2013-04-08
Cited: 9
Clicked: 6605
Ling Zhao, You-bin Wang, Shi-rui Qin, Xue-mei Ma, Xue-jun Sun, Ming-lian Wang, Ru-gang Zhong. Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap[J]. Journal of Zhejiang University Science B, 2013, 14(5): 382-391.
@article{title="Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap",
author="Ling Zhao, You-bin Wang, Shi-rui Qin, Xue-mei Ma, Xue-jun Sun, Ming-lian Wang, Ru-gang Zhong",
journal="Journal of Zhejiang University Science B",
volume="14",
number="5",
pages="382-391",
year="2013",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1200317"
}
%0 Journal Article
%T Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap
%A Ling Zhao
%A You-bin Wang
%A Shi-rui Qin
%A Xue-mei Ma
%A Xue-jun Sun
%A Ming-lian Wang
%A Ru-gang Zhong
%J Journal of Zhejiang University SCIENCE B
%V 14
%N 5
%P 382-391
%@ 1673-1581
%D 2013
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1200317
TY - JOUR
T1 - Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap
A1 - Ling Zhao
A1 - You-bin Wang
A1 - Shi-rui Qin
A1 - Xue-mei Ma
A1 - Xue-jun Sun
A1 - Ming-lian Wang
A1 - Ru-gang Zhong
J0 - Journal of Zhejiang University Science B
VL - 14
IS - 5
SP - 382
EP - 391
%@ 1673-1581
Y1 - 2013
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1200317
Abstract: Objective: Skin damage induced by ischemia/reperfusion (I/R) is a multifactorial process that often occurs in plastic surgery. The mechanisms of I/R injury include hypoxia, inflammation, and oxidative damage. Hydrogen gas has been reported to alleviate cerebral I/R injury by acting as a free radical scavenger. Here, we assessed the protective effect of hydrogen-rich saline (HRS) on skin flap I/R injury. Methods: Abdominal skin flaps of rats were elevated and ischemia was induced for 3 h; subsequently, HRS or physiological saline was administered intraperitoneally 10 min before reperfusion. On postoperative Day 5, flap survival, blood perfusion, the accumulation of reactive oxygen species (ROS), and levels of cytokines were evaluated. Histological examinations were performed to assess inflammatory cell infiltration. Results: Skin flap survival and blood flow perfusion were improved by HRS relative to the controls. The production of malondialdehyde (MDA), an indicator of lipid peroxidation, was markedly reduced. A multiplex cytokine assay revealed that HRS reduced the elevation in the levels of inflammatory cytokines, chemokines and growth factors, with the exception of RANTES (regulated on activation, normal T-cell expressed and secreted) growth factor. HRS treatment also reduced inflammatory cell infiltration induced by I/R injury. Conclusions: Our findings suggest that HRS mitigates I/R injury by decreasing inflammation and, therefore, has the potential for application as a therapy for improving skin flap survival.
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