Preservation on calcium homeostasis is involved in mitochondrial protection of Limonium sinense against liver damage in mice

    Authors

    X. H. Tang; J. Chen; X. L. Yang; L. F. Yan;J. Gao

    Comments

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    Abbreviated Journal Title

    Pharmacogn. Mag.

    Keywords

    D-galactosamine; Limonium sinense (Girard) Ktze; lipopolysaccharide; mitochondrial Ca(2+)-ATPase activity; mitochondrial Ca(2+) overload; PERMEABILITY TRANSITION; CARBON-TETRACHLORIDE; INJURY; ACID; HEPATOPROTECTION; INTOXICATION; INHIBITION; MECHANISMS; APOPTOSIS; CULTURE; Chemistry, Medicinal

    Abstract

    Mechanisms underlying the mitochondrial protection of Limonium sinense extracts (LSE) was studied in lipopolysaccharide and D-galactosamine (LPS/D-GalN) intoxicated mice. It was found that increased activities of serum aspartate aminotransferase and alanine aminotransferase induced by LPS/D-GalN were significantly inhibited by pretreatment with LSE. The obvious disruption of membrane potential, intramitochondrial Ca(2+) overload and suppression in mitochondrial Ca(2+)-ATPase activity induced by LPS/D-GalN were significantly blocked by pretreatment with LSE. It was concluded that mechanisms underlying protection of LSE against liver mitochondria damage might be related to the preservation on mitochondrial Ca(2+) homeostasis through the preservation on mitochondrial Ca(2+)-ATPase activity.

    Journal Title

    Pharmacognosy Magazine

    Volume

    6

    Issue/Number

    23

    Publication Date

    1-1-2010

    Document Type

    Article

    Language

    English

    First Page

    191

    Last Page

    197

    WOS Identifier

    WOS:000283486200010

    ISSN

    0973-1296

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