Hydrogen Water Protects Brain After Cardiac Arrest in Rats
- Authors
- Lin Zhao, Lu Zhang, Pan Yu, Yu Gao, Lin Wu, Manlin Duan, Jianguo Xu
- Journal
- National Medical Journal of China
- Year
- 2015
- DOI
- 10.3760/cma.j.issn.0376-2491.2015.06.014
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Cerebral Ischemia-Reperfusion Injury
- Body System
- Nervous System
TL;DR
Hydrogen-rich saline may help reduce brain damage after a stroke by decreasing harmful protein activity in rats.
Key Finding
Hydrogen-rich saline reduced brain damage and improved neurological outcomes in rats with global cerebral ischemia-reperfusion injury by inhibiting the JNK-FOXO3A cellular damage pathway.
Summary
This study tested whether hydrogen-rich saline could protect rat brains from damage caused by temporary loss of blood flow during cardiac arrest. Researchers induced cardiac arrest in rats, then gave some animals hydrogen-rich saline injections while others received regular saline. They found that hydrogen-rich saline reduced brain cell death in the hippocampus (a memory-related brain region) and improved neurological function, possibly by blocking a specific cellular damage pathway called JNK-FOXO3A.
Practical Takeaway
This rat study suggests hydrogen-rich saline may have neuroprotective potential for brain injuries related to cardiac arrest, but these findings cannot yet be applied to humans. Much more research, including human clinical trials, would be needed before any therapeutic claims could be made.
Abstract
To investigate the role of FOXO3a in process of hydrogen-rich saline attenuating global cerebral ischemia-reperfusion (I/R) injury in rats. Seventy-two male Sprague Dawley rats, weighing 280-320 g, were randomly divided into six groups (n = 12 each) : sham operation group (group I), cerebral ischemia-reperfusion group (group II), hydrogen-rich saline group (group III), vehicle group (group IV), JNK inhibitor SP600125 group (group V), JNK inhibitor+hydrogen-rich saline group (group VI). Global cerebral I/R was produced by transesophageal pacing inducing cardiac arrest (CA) method. Cardiopulmonary resuscitation (CPR) and mechanical ventilation was implemented at the end of 4 min for CA. In groups III and VI, hydrogen-rich saline 5 ml/kg was intraperitoneally immediately and 6 hours after reperfusion, while equel volume of nomal saline was injected in the other four groups. The rats in groups V and VI received intracerebroventricular injection of JNK inhibitor SP600125 10 µl 30 min before ischemia, while group IV received intracerebroventricular injection of equal volume of DMSO. Neuro Deficit Score (NDS) was evaluated at 24 h of reperfusion. Then rats were sacrificed, and the global brain tissues were obtained and stained with HE for examination of the changes in pyramidal cells in the CA1 region of hippocampus. The bilateral hippocampi were romoved for detection of the expression of p-JNK, JNK and FOXO3a using Western Blotting. Compared with group I, the expression of p-JNK, nuclear FOXO3a and the level of NDS were significantly up-regulated, and the number of pyramidal cells and was decreased in group II and IV. Compared with group II, the expression of p-JNK, nuclear FOXO3a and the level of NDS were significantly down-regulated, and the number of pyramidal cells was increased in group III, V and VI. Hydrogen-rich saline can attenuate global cerebral I/R injure through inhibiting JNK, reducing the expression of FOXO3a.