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Inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge.

Inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge. Research Abstract Details 

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  • Inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge. Abstract Text:

    jia-ping zhangJia-Ping Zhang,xi yingXi Ying,yu chenYu Chen,zong-cheng yangZong-Cheng Yang,yue-sheng huangYue-Sheng Huang,jia-ping zhangJia-Ping Zhang,xi yingXi Ying,yu chenYu Chen,zong-cheng yangZong-Cheng Yang,yue-sheng huangYue-Sheng Huang,

    This study was aimed to investigate the effects of SB203580, the specific p38 mitogen-activated protein (MAP) kinase inhibitor, on cardiac myocyte survival and secretion of cytokines in an in vitro model of hypoxia and burn serum challenge. Results demonstrated that hypoxia and burn serum induced a persistent activation of p38 MAP kinase in primary cultured neonatal rat cardiomyocytes during the 12h period of stimulation, concomitant with a time-dependent increased expression of tumor necrosis factor (TNF)-alpha and inducible nitric oxide (iNOS), a progressively developed oxidative stress reflected by malondialdehyde (MDA) production, and myocytes injury evidenced by the increased levels of released lactate dehydrogenase (LDH) and the decreased myocyte viability. Furthermore, hypoxia and burn serum resulted in a significant increase in myocyte apoptosis, which may account for the impairment of myocyte viability as observed. SB203580 abolished p38 MAP kinase activation, blunted the upregulation of TNF-alpha, iNOS and the subsequent nitric oxide (NO) production, reduced oxidative stress, and alleviated hypoxia and burn serum-induced myocytes injury or apoptosis. These results demonstrated for the first time that inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge possibly via reducing the production of cytokines, such as TNF-alpha and NO, and the subsequent oxidative stress, providing strong evidence that the excessive inflammatory cytokines produced by cardiomyocytes themselves may be sufficient to cause myocardial injury after burn.

    Inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge. Publishing Authors By Initials

    jp zhangJP Zhang,x yingX Ying,y chenY Chen,zc yangZC Yang,ys huangYS Huang,jp zhangJP Zhang,x yingX Ying,y chenY Chen,zc yangZC Yang,ys huangYS Huang,

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    PUBMED ID PMID:

    MEDLINE DATE:

    Inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Burns : journal of the International Society for B

    VOLUME: 34

    Page Numbers: 220-7

    Journal Abbreviation:

    ISSN: 0305-4179

    DAY: 10

    MONTH: 08

    YEAR: 2007

    Inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge. Information

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    LANGUAGE: eng

    NlmUniqueID: 8913178

    Inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge. Keywords Mesh Terms:

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    Grant and Affiliation Information for Inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge.

    AFFILIATION: State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Burns, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.

    Country: England

    England Research PublicationEngland Research Publication

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    MEDLINETA: Burns

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