Abstract
ABSTRACTPurpose:Subarachnoid hemorrhage (SAH) is a common complication of cerebral vascular disease. Hydrogen has been reported to alleviate early brain injury (EBI) through oxidative stress injury, reactive oxygen species (ROS), and autophagy. Autophagy is a programmed cell death mechanism that plays a vital role in neuronal cell death after SAH. However, the precise role of autophagy in hydrogen-mediated neuroprotection following SAH has not been confirmed.Methods:In the present study, the objective was to investigate the neuroprotective effects and potential molecular mechanisms of hydrogen-rich saline in SAH-induced EBI by regulating neural autophagy in the C57BL/6 mice model. Mortality, neurological score, brain water content, ROS, malondialdehyde (MDA), and neuronal death were evaluated.Results:The results show that hydrogen-rich saline treatment markedly increased the survival rate and neurological score, increased neuron survival, downregulated the autophagy protein expression of Beclin-1 and LC3, and endoplasmic reticulum (ER) stress. That indicates that hydrogen-rich saline-mediated inhibition of autophagy and ER stress ameliorate neuronal death after SAH. The neuroprotective capacity of hydrogen-rich saline is partly dependent on the ROS/Nrf2/heme oxygenase-1 (HO-1) signaling pathway.Conclusions:The results of this study demonstrate that hydrogen-rich saline improves neurological outcomes in mice and reduces neuronal death by protecting against neural autophagy and ER stress.
Highlights
Subarachnoid hemorrhage (SAH) is a common complication of cerebral vascular disease that is associated with a high rate of mortality, morbidity, and poor prognosis, especially in patients with hypertension
No significant differences between the three groups. (b) SAH grade scores in the sham group, the SAH group, and the SAH + HS group, which showed no significant differences
The results showed that SAH increased the brain water content significantly (p
Summary
Subarachnoid hemorrhage (SAH) is a common complication of cerebral vascular disease that is associated with a high rate of mortality, morbidity, and poor prognosis, especially in patients with hypertension. The key causes for SAH patients’ poor outcomes were early brain damage (EBI) and cerebral vasospasm (CVS)[4]. Recent clinical trials have shown that drugs can greatly reduce CVS while having little impact on outcomes following SAH5, and previous clinical studies demonstrated it too[6]. The latest research has shown that EBI after SAH appears to play a critical role[7,8,9,10]. The possible mechanisms underlying EBI include autophagy, apoptosis, direct neuronal death, and necroptosis[8,11,12,13]. Inhibitors of ferroptosis defended against toxicity caused by hemoglobin and hemin. To date, it is unknown how often various types of cell death play a role in SAH-induced toxicity
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