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Protective effects of hyperbaric oxygen preconditioning against LPS-induced acute lung injury in rats
被引:0
|作者:
Bai, Chongfeng
[1
,2
]
Li, Tao
[2
]
Chen, Yi
[3
]
Xu, Tongyi
[2
]
Wang, Xiaohong
[4
]
Yu, Jinjian
[2
]
Liu, Xuan
[5
]
Wang, Yun
[2
]
Sun, Qing
[3
]
机构:
[1] Qingdao Univ, Postdoctoral Res Stn, Qingdao, Peoples R China
[2] 401 Hosp Peoples Liberat Army, Dept Cardiothorac Surg, Qingdao 266071, Peoples R China
[3] 401 Hosp Peoples Liberat Army, Dept Med Imaging, Qingdao 266071, Peoples R China
[4] 401 Hosp Peoples Liberat Army, Dept Hyperbar Med, Qingdao 266071, Peoples R China
[5] Hosp 92196 Unit Chinese Navy, Qingdao 266071, Peoples R China
关键词:
HBO2;
preconditioning;
acute lung injury;
nuclear factor erythroid 2-related factor 2 (Nrf2);
heme-oxygenase 1 (HO-1);
NF-KAPPA-B;
ISCHEMIA-REPERFUSION INJURY;
FOCAL CEREBRAL-ISCHEMIA;
OXIDATIVE STRESS;
ANTIOXIDANT ENZYMES;
UP-REGULATION;
NRF2;
INFLAMMATION;
TOLERANCE;
ACTIVATION;
D O I:
暂无
中图分类号:
Q17 [水生生物学];
学科分类号:
071004 ;
摘要:
Introduction: Acute lung injury (ALI) is generally caused by oxidative damages and pulmonary overinflammations. Hyperbaric oxygen preconditioning (HBO2 -PC) has been proven protective against oxidative-stress-related injuries. In this study, we investigated the effect of HBO2 -PC on lipopolysaccharide (LPS)-induced ALI in rats. Methods: Thirty-two Sprague-Dawley rats randomly assigned into Sham, HBO2-PC, ALI and HBO2 -PC+ALI groups (eight in each group) were sacrificed at 12 hours after the injection of LPS. The severity of ALI in rats was assessed in terms of histopathological changes in addition to wet/dry weight ratios. The levels of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6 and IL-1 beta in serum and lung homogenates were measured by enzyme-linked immunosorbent and qRT-PCR assays. Activities by hydrogen peroxide (H2O2), malondialdehyde (MDA), myeloperoxidase (MPO) as well as superoxide dismutase (SOD) in rat lungs were tested for neutrophil infiltration. Meanwhile the oxidative stress molecular markers nuclear factorkappa B(NF-kappa B) p65 and nuclear factor erythroid 2-related factor 2 (Nrf2), together with its downstream heme-oxygenase 1 (HO-1) and NAD(P)H: quinone oxidoreductase I (NQO1) were also quantified. Results: HBO2 -PC significantly alleviated LPS-induced ALI, lowered the lung injury scores, reduced lung water content, and reduced H2O2 , MDA levels as well as MPO activity, while simultaneously improving the arterial partial oxygen pressure (PaO2 ) and SOD activity. Furthermore, HBO2 -PC inhibited the nuclear translocation of NF-kappa B p65 while enhancing the nuclear translocation of Nrf2, thus upregulating HO-1 and NQO1. Conclusions: Our results suggest that HBO2-PC was potentially protective for LPS-induced ALI lungs in rats, with a presumed mechanism that suppressed NF-kappa B while activating Nrf2. We propose that HBO2 -PC should be considered a potential therapeutic strategy against ALI in rats.
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页码:323 / 333
页数:11
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