Hydrogen-rich Saline Group Research Articles

Hydrogen-Rich Saline Protects Against Acute Lung Injury Induced by Extensive Burn in Rat Model

Hydrogen has been reported to selectively quench detrimental reactive oxygen species, particularly hydroxyl radical, and to prevent myocardial or hepatic ischemia/reperfusion injury in multiple models. The aim of this study is to investigate whether hydrogen protects against severe burn-induced acute lung injury in rats. Rats were divided into four groups: sham plus normal saline, burn injury plus normal saline, burn injury plus hydrogen-rich saline, and burn injury plus edaravone. Animals were given full-thickness burn wounds (30% TBSA) using boiling water, except the sham group that was treated with room temperature water. The rats in hydrogen group received 5 ml/kg of hydrogen-rich saline, sham and burn controls obtained the same amount of saline, and the edaravone group was treated with 9 mg/kg of edaravone in saline. Lactated Ringer's solution was given at 6 hours postburn. The lungs were harvested 12 hours postburn for laboratory investigations. Severe burns with delayed resuscitation rapidly caused lung edema and impaired oxygenation in rats. These dysfunctions were ameliorated by administration of hydrogen-rich saline or edaravone. When compared with the burn injury plus normal saline group, hydrogen-rich saline or edaravone group significantly attenuated the pulmonary oxidative products, such as malondialdehyde, carbonyl, and 8-hydroxy-2'-deoxyguanosine. Furthermore, administration of hydrogen-rich saline or edaravone dramatically reduced the pulmonary levels of pulmonary inflammation mediators and myeloperoxidase. Intraperitoneal administration of hydrogen-rich saline improves pulmonary function by reducing oxidative stress and inflammatory response in severe burn-induced acute lung injury.

A comparison of the take-off measured under laboratory and jumping-hill conditions

To investigate the potential beneficial effect of hydrogen-rich saline (HRS) in ischemia–reperfusion (IR) injury of skeletal muscle.Three experimental groups were established in male Sprague–Dawley rats: (1) sham group, (2) IR with normal saline group, (3) and IR with HRS group. A rat model of skeletal muscle IR injury was induced by 3-h tourniquet occlusion on its left hind limb and 4-h reperfusion. Normal saline and HRS (1.0 mL/100 g) were administered intraperitoneally at 10 min before reperfusion, respectively. Muscle and serum samples were analyzed for detecting the levels of myeloperoxidase (MPO), superoxide dismutase (SOD), malondialdehyde (MDA), and hydroxyl radical (•OH). Muscle samples were assessed by wet/dry rate, hematoxylin and eosin histologic assessment, Bcl2, Bax, cytochrome C, LC3B, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling, and electron microscopy.The wet/dry ratio increased significantly in the IR group (P < 0.01 compared with that in the sham group) and decreased significantly in IR with HRS groups (4.12 ± 0.14 versus 4.12 ± 0.14, P < 0.01 compared with that in the IR group). Muscle tissues and serum of the IR group had significantly increased levels of MPO, MDA, •OH content, and decreased SOD activities compared with the sham group (P < 0.01). The activity of SOD in the IR with HRS group was greatly elevated compared with that in the IR group (295.028 ± 9.288 versus 249.190 ± 5.450 in muscle tissues; 91.627 ± 2.604 versus 73.4045 ± 6.487 in serum; P < 0.01), whereas the levels of MPO, MDA, and •OH content were clearly reduced (MPO: 0.5649 ± 0.0724 versus 1.0984 ± 0.0824 in muscle tissues; 0.7257 ± 0.1232 versus 1.3147 ± 0.0531 in serum. MDA: 4.457 ± 0.650 versus 7.107 ± 0.597 in muscle tissues; 2.531 ± 0.434 versus 4.626 ± 0.237 in serum. •OH: 16.451 ± 0.806 versus 19.871 ± 0.594 in muscle tissues; 500.212 ± 7.387 versus 621.352 ± 7.591 in serum, P < 0.01). The integrated optical density of positive amethyst staining increased significantly in the IR group (P < 0.01 compared with that in the sham group) and decreased significantly in IR with HRS group (928.79 ± 234.537 versus 3005.972 ± 83.567, P < 0.01 compared with that in the IR group). Muscle tissues of the IR group had significantly increased levels of Bax, cytochrome C, LC3B content, and decreased Bcl2 activities compared with those in the sham group (P < 0.01). The activity of Bcl2 in the IR with HRS group was greatly elevated compared with that in the IR group (0.2635 ± 0.0704 versus 0.1242 ± 0.0662; P < 0.01), whereas the levels of Bax, cytochrome C, and LC3B content were clearly reduced (Bax: 0.3103 ± 0.0506 versus 0.5122 ± 0.0148; cytochrome C: 0.4194 ± 0.1116 versus 0.8127 ± 0.0166; LC3B: 0.5884 ± 0.0604 versus 1.3758 ± 0.0319; respectively, P < 0.01).HRS seems to be effective in attenuating IR injury in skeletal muscle via its antioxidant, anti-apoptosis, and anti-autophagy effect.