Effects of Hydrogen Sulfide on a Rat Model of Sepsis-associated Encephalopathy
To investigate the interaction and involvement of sodium hydrosulfide (NaHS), a H2S donor, on hippocampus of rats suffering from sepsis-associated encephalopathy, rats were subjected to cecal ligation and puncture (CLP)-induced sepsis. Adult male Sprague-Dawley rats were randomly divided into four g...
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| Published in | Journal of Huazhong University of Science and Technology. Medical sciences Vol. 31; no. 5; pp. 632 - 636 |
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| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
Heidelberg
Huazhong University of Science and Technology
01.10.2011
Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China%Department of Emergency, the Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1672-0733 1993-1352 |
| DOI | 10.1007/s11596-011-0573-2 |
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| Summary: | To investigate the interaction and involvement of sodium hydrosulfide (NaHS), a H2S donor, on hippocampus of rats suffering from sepsis-associated encephalopathy, rats were subjected to cecal ligation and puncture (CLP)-induced sepsis. Adult male Sprague-Dawley rats were randomly divided into four groups: Sham group, CLP group, CLP+NaHS group and CLP+aminooxyacetic acid (AOAA, an inhibitor of H2S formation) group. The four groups were observed at 3, 6, 9, 12 h after treatment. We examined hippocampal H2S synthesis and the expression of cystathionine-β-synthetase (CBS), a major enzyme involved in the H2S synthesis in hippocampus. CBS expression was detected by reverse transcription polymerase chain reaction (RT-PCR). The concentrations of inflammatory cytokines (TNF-α, IL-1β) were determined in hippocampus by using enzyme-linked immunosorbent assay (ELISA). Neuronal damage was studied by histological examination of hippocampus. In CLP group, H2S synthesis was significantly increased in hippocampus compared with sham group and it peaked 3 h after CLP (P〈0.05). Sepsis also resulted in a significantly upregulated CBS mRNA in hippocampus. The levels of TNF-α and IL-1β in the hippocampus were substantially elevated at each time point of measurement (P〈0.05), and they also reached a peak value at about 3 h. Administration of NaHS significantly aggravated sepsis-associated hippocampus inflammation, as evidenced by TNF-α and IL-1β activity and histological changes in hippocampus. In septic rats pretreated with AOAA, sepsis-associated hippocampus inflammation was reduced. It is concluded that the rats subjected to sepsis may suffer from brain injury and elevated pro-inflammatory cytokines are responsible for the process. Furthermore, administration of H2S can increase injurious effects and treatment with AOAA can protect the brain from injury. |
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| Bibliography: | To investigate the interaction and involvement of sodium hydrosulfide (NaHS), a H2S donor, on hippocampus of rats suffering from sepsis-associated encephalopathy, rats were subjected to cecal ligation and puncture (CLP)-induced sepsis. Adult male Sprague-Dawley rats were randomly divided into four groups: Sham group, CLP group, CLP+NaHS group and CLP+aminooxyacetic acid (AOAA, an inhibitor of H2S formation) group. The four groups were observed at 3, 6, 9, 12 h after treatment. We examined hippocampal H2S synthesis and the expression of cystathionine-β-synthetase (CBS), a major enzyme involved in the H2S synthesis in hippocampus. CBS expression was detected by reverse transcription polymerase chain reaction (RT-PCR). The concentrations of inflammatory cytokines (TNF-α, IL-1β) were determined in hippocampus by using enzyme-linked immunosorbent assay (ELISA). Neuronal damage was studied by histological examination of hippocampus. In CLP group, H2S synthesis was significantly increased in hippocampus compared with sham group and it peaked 3 h after CLP (P〈0.05). Sepsis also resulted in a significantly upregulated CBS mRNA in hippocampus. The levels of TNF-α and IL-1β in the hippocampus were substantially elevated at each time point of measurement (P〈0.05), and they also reached a peak value at about 3 h. Administration of NaHS significantly aggravated sepsis-associated hippocampus inflammation, as evidenced by TNF-α and IL-1β activity and histological changes in hippocampus. In septic rats pretreated with AOAA, sepsis-associated hippocampus inflammation was reduced. It is concluded that the rats subjected to sepsis may suffer from brain injury and elevated pro-inflammatory cytokines are responsible for the process. Furthermore, administration of H2S can increase injurious effects and treatment with AOAA can protect the brain from injury. 42-1679/R hydrogen sulfide sepsis-associated encephalopathy TNF-α IL-1β ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
| ISSN: | 1672-0733 1993-1352 |
| DOI: | 10.1007/s11596-011-0573-2 |