Abstract:
BACKGROUND:Myocardial apoptosis is involved in the pathogenesis of sepsis-related myocardial depression. However, the underlying mechanism remains unknown. This study investigated the role of mitochondrial damage and mitochondria-induced oxidative stress during cardiac apoptosis in septic rats. METHODS:Seventy-two Sprague-Dawley rats were randomly divided into a control group and septic group receiving lipopolysaccharide injection. Heart tissue was removed and changes in cardiac morphology were observed by light microscopy and scanning electron microscopy. In situ apoptosis was examined using terminal transferase-mediated dUTP nick end-labeling assay and nuclear factor-kappa B activation in myocardium by Western blotting to estimate myocardial apoptosis. Appearance of mitochondrial cristae and activation of cytochrome C oxidase were used to evaluate mitochondrial damage. Oxidative stress was assessed by mitochondrial lipid and protein oxidation, and antioxidant defense was assessed by mitochondrial superoxide dismutase and glutathione peroxidase activity. RESULTS:Sepsis-induced inflammatory cell infiltration, myocardium degeneration and dropsy were time-dependent. Expanded capillaries were observed in the hearts of infected rats 24 hours post-challenge. Compared with sham-treated rats, the percentage of cell apoptosis increased in a time-dependent manner in hearts from septic rats at 6 hours, 12 hours and 24 hours post-injection (P < 0.05). The expression of nuclear factor-kappa B p65 decreased gradually in the cytosol and increased in the nucleus during sepsis, indicating that septic challenge provoked the progressive activation of nuclear factor-kappa B. Mitochondrial cristae and activation of cytochrome C oxidase increased in a time-dependent manner. Both superoxide dismutase and glutathione peroxidase activities decreased, while mitochondrial lipid and protein oxidation increased between 6 and 24 hours after lipopolysaccharide challenge. CONCLUSIONS:Septic challenge induced myocardial apoptosis and mitochondrial damage. Furthermore, mitochondrial damage via alteration of defenses against reactive oxygen species might play an important role in myocardial apoptosis during sepsis.
journal_name
Chin Med J (Engl)journal_title
Chinese medical journalauthors
Li L,Hu BC,Chen CQ,Gong SJ,Yu YH,Dai HW,Yan Jsubject
Has Abstractpub_date
2013-01-01 00:00:00pages
1860-6issue
10eissn
0366-6999issn
2542-5641journal_volume
126pub_type
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journal_title:Chinese medical journal
pub_type: 杂志文章,评审
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journal_title:Chinese medical journal
pub_type: 杂志文章
doi:
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journal_title:Chinese medical journal
pub_type: 杂志文章
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journal_title:Chinese medical journal
pub_type: 杂志文章
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doi:
更新日期:2006-04-20 00:00:00
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更新日期:2008-03-05 00:00:00
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pub_type: 杂志文章
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更新日期:2015-01-20 00:00:00
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pub_type: 杂志文章,随机对照试验
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更新日期:2016-06-05 00:00:00
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journal_title:Chinese medical journal
pub_type: 杂志文章
doi:
更新日期:2013-02-01 00:00:00
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pub_type: 杂志文章
doi:
更新日期:1989-06-01 00:00:00
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pub_type: 杂志文章
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更新日期:2011-02-01 00:00:00
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pub_type: 杂志文章
doi:
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pub_type: 杂志文章,meta分析
doi:
更新日期:2013-01-01 00:00:00
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doi:
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pub_type: 临床试验,杂志文章,随机对照试验
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