Molecular hydrogen alleviates brain injury and cognitive impairment in a chronic sequelae model of murine polymicrobial
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RESEARCH ARTICLE
Molecular hydrogen alleviates brain injury and cognitive impairment in a chronic sequelae model of murine polymicrobial sepsis Yi Jiang1,2 · Kai Zhang1,2 · Yang Yu1,2 · Yaoqi Wang1,2 · Naqi Lian1,2 · Keliang Xie1,2 · Yonghao Yu1,2 Received: 30 May 2020 / Accepted: 6 October 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Sepsis-related encephalopathy (SAE), which causes a series of brain injuries and long-term, potentially irreversible cognitive dysfunction, is closely associated with increased morbidity and mortality. Hydrogen ( H2) is a new type of medical gas molecule that has been widely used in the treatment of various diseases in recent years. The aim of the present study was to explore the protective effects of H 2 inhalation on brain injury and long-term cognitive impairment in an improved chronic septic mouse model. Male C57BL/6J mice were randomized into four groups: Control, Control + H2, SAE and SAE + H2. The SAE and Control models were established by intraperitoneal injection of human stool suspension or saline in mice. H 2 (2%) was inhaled for 60 min at 1 h and 6 h after SAE or Control treatment. The survival rates were recorded for 14 days (days 1–14) and the Morris Water Maze was performed for 7 days (days 8–14). To assess the severity of the brain injury, hematoxylin and eosin staining, Nissl staining, Evans blue (EB) extravasation and the wet/dry weight ratio of brain tissue were detected 24 h after SAE or Control treatment. In addition, inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin 6 (IL-6), high-mobility group box 1 (HMGB1), as well as the protein levels of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), zonula occludens-1 (ZO-1) and Occludin, were measured 6, 12 and 24 h after SAE or Control treatment. The results showed that H2 treatment increased survival rates, mitigated cognitive impairment, reduced hippocampal histological damage, decreased EB and water content, and decreased the levels of TNF-α, IL-6, HMGB1, Nrf2, HO-1, ZO-1 and Occludin, as compared with the SAE group. These data revealed that 2% H 2 could suppress brain damage and improve cognitive function in septic mice by inhibiting oxidative stress, inflammatory response and the sepsis-induced blood–brain barrier (BBB) disruption. Keywords Sepsis-associated encephalopathy · Hydrogen · Blood brain barrier · Neuroinflammation · Oxidative stress
Introduction Sepsis remains the leading cause of mortality in the intensive care unit, and yet few proven therapeutic strategies for it exist (Zhou et al. 2017). Sepsis-related encephalopathy Communicated by Sreedharan Sajikumar. * Yang Yu [email protected] * Yonghao Yu [email protected] 1
Department of Anesthesiology, Tianjin Medical University General Hospital, No. 154 Anshan Road, Tianjin 300052, People’s Republic of China
Tianjin Institute of Anesthesiology, Tianjin 300052, People’s Republic of China
2
(SAE) is a common complication of sepsis that is caused by
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