General Research
Model: rat
Hydrogen Inhalation Attenuates Oxidative Stress Related Endothelial Cells Injury After Subarachnoid Hemorrhage in Rats
Simplified Version Available
How Hydrogen Inhalation Could Help Prevent Brain Damage After Hemorrhage
Researchers in China have found that hydrogen inhalation can reduce brain damage in rats with subarachnoid hemorrhage. The study's findings are promising and could lead to new treatments for people who have suffered a hemorrhage. Hydrogen inhalation has antioxidant properties that can neutralize harmful chemicals and reduce oxidative stress.
Read Simplified ArticleAbstract
Publish Year 2020 Country China Rank Positive Journal Frontiers in Neuroscience Primary Topic Brain Secondary TopicBrain Injury Model Rat Tertiary TopicIntracranial Hemorrhage Vehicle Gas pH N/A Application Inhalation Comparison Complement
Background
Methods: One hundred eighty-two male SD rats were used for the study. SAH was induced by endovascular perforation. H2 at a concentration of 3.3% was inhaled beginning at 0.5 h after SAH for duration of 30, 60 or 120 min, followed by single administration or once daily administration for 3 days. The temporal expression of NLRP3 and ASC in the brain was determined, with the effect of hydrogen inhalation evaluated. In addition, brain water content, oxidative stress markers, inflammasome, apoptotic markers, microthrombosis, and vasospasm were evaluated at 24 or 72 h after SAH.
Methods
Results: The expression of NLRP3 and ASC were upregulated after SAH associated with elevated expression of MDA, 8-OHdG, 4-HNE, HO-1, TLR4/NF-κB, inflammatory and apoptotic makers. Hydrogen inhalation reduced the expression of these inflammatory and apoptotic makers in the vessels, brain edema, microthrombi formation, and vasospasm in rats with SAH relative to control. Hydrogen inhalation also improved short-term and long-term neurological recovery after SAH.
Results
Conclusion: Hydrogen inhalation can ameliorate oxidative stress related endothelial cells injury in the brain and improve neurobehavioral outcomes in rats following SAH. Mechanistically, the above beneficial effects might be related to, at least in part, the inhibition of activation of ROS/NLRP3 axis.