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• W4310295903 abstract "Abstract Background Sepsis-associated encephalopathy (SAE) is one of the most common types of sepsis-related organ dysfunction without overt central nervous system (CNS) infection. It is associated with higher mortality, low quality of life, and long-term neurological sequelae in suspected patients. At present there is no specific treatment for SAE rather than supportive therapy and judicious use of antibiotics, which are sometimes associated with adverse effects. Molecular hydrogen (H2) has been reported to play crucial role in regulating inflammatory responses, neuronal injury, apoptosis and mitochondrial dysfunction in adult models of SAE. Here we report the protective effect of hydrogen-rich saline in juvenile SAE rat model and its possible underling mechanism(s). Materials and methods Rats were challenged with lipopolysaccharide (LPS) at a dose of 8 mg/kg injected intraperitoneally to induce sepsis and hydrogen-rich saline (HRS) administered 1 h following LPS induction at a dose of 5 ml/kg. Rats were divided into: sham, sham + HRS, LPS and LPS + HRS. At 48 h, rats were sacrificed and Nissl staining for neuronal injury, TUNEL assay for apoptotic cells detection, immunohistochemistry, and ELISA protocol for inflammatory cytokines determination, mitochondrial dysfunction parameters, electron microscopy and western blot analysis were studied to examine the effect of HRS in LPS-induced septic rats. Results Rats treated with HRS improved neuronal injury, improvement in rats’ survival rate. ELISA analysis showed decreased TNF-α and IL-1β and increased IL-10 expression levels in the HRS-treated group. Apoptotic cells were decreased after HRS administration in septic rats. The numbers of GFAP and IBA-1positive cells were attenuated in the HRS-treated group when compared to the LPS group. Subsequently, GFAP and IBA-1 immunoreactivity were decreased after HRS treatment. Mitochondrial membrane potential detected by JC-1 dye and ATP content were decreased in septic rats, which were improved after HRS treatment, while release of ROS was increased in the LPS group reverted by HRS treatment, ameliorating mitochondrial dysfunction. Further analysis by transmission electron microscopy showed decreased number of mitochondria and synapses, and disrupted mitochondrial membrane ultrastructure in the LPS group, while HRS administration increased mitochondria and synapses number. Conclusion These data demonstrated that HRS can improve survival rate, attenuate neuroinflammation, astrocyte and microglial activation, neuronal injury and mitochondrial dysfunction in juvenile SAE rat model, making it a potential therapeutic candidate in treating paediatric SAE." @default.
• W4310295903 created "2022-11-30" @default.
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• W4310295903 date "2022-11-26" @default.
• W4310295903 modified "2023-10-01" @default.
• W4310295903 title "Effects of hydrogen-rich saline in neuroinflammation and mitochondrial dysfunction in rat model of sepsis-associated encephalopathy" @default.
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• W4310295903 cites W1964502026 @default.
• W4310295903 cites W1983687844 @default.
• W4310295903 cites W2007330771 @default.
• W4310295903 cites W2029520101 @default.
• W4310295903 cites W2031706510 @default.
• W4310295903 cites W2032861830 @default.
• W4310295903 cites W2035673027 @default.
• W4310295903 cites W2043874394 @default.
• W4310295903 cites W2051135672 @default.
• W4310295903 cites W2055497959 @default.
• W4310295903 cites W2087578679 @default.
• W4310295903 cites W2094461058 @default.
• W4310295903 cites W2139535523 @default.
• W4310295903 cites W2139871065 @default.
• W4310295903 cites W2143456439 @default.
• W4310295903 cites W2159641317 @default.
• W4310295903 cites W2167061515 @default.
• W4310295903 cites W2169657429 @default.
• W4310295903 cites W2170596494 @default.
• W4310295903 cites W2173599989 @default.
• W4310295903 cites W2192729786 @default.
• W4310295903 cites W2399688998 @default.
• W4310295903 cites W2410719073 @default.
• W4310295903 cites W2436152379 @default.
• W4310295903 cites W2559943991 @default.
• W4310295903 cites W2572710398 @default.
• W4310295903 cites W2600496322 @default.
• W4310295903 cites W2613603483 @default.
• W4310295903 cites W2745212246 @default.
• W4310295903 cites W2750534773 @default.
• W4310295903 cites W2779809707 @default.
• W4310295903 cites W2782351989 @default.
• W4310295903 cites W2891403276 @default.
• W4310295903 cites W2912627959 @default.
• W4310295903 cites W2917522876 @default.
• W4310295903 cites W2940220126 @default.
• W4310295903 cites W2941269498 @default.
• W4310295903 cites W2947934753 @default.
• W4310295903 cites W2956031447 @default.
• W4310295903 cites W2967095202 @default.
• W4310295903 cites W2980959244 @default.
• W4310295903 cites W3001022241 @default.
• W4310295903 cites W3001334548 @default.
• W4310295903 cites W3003568098 @default.
• W4310295903 cites W3004285897 @default.
• W4310295903 cites W3005429114 @default.
• W4310295903 cites W3005592155 @default.
• W4310295903 cites W3006241683 @default.
• W4310295903 cites W3007926685 @default.
• W4310295903 cites W3009869083 @default.
• W4310295903 cites W3011928031 @default.
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• W4310295903 cites W3112352280 @default.
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• W4310295903 cites W3158924207 @default.
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• W4310295903 doi "https://doi.org/10.1186/s12967-022-03746-4" @default.
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