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Effect of propofol on hypoxia re‐oxygenation induced neuronal cell damage in vitro *
Author(s) -
Huang Y.,
Zitta K.,
Bein B.,
Scholz J.,
Steinfath M.,
Albrecht M.
Publication year - 2013
Publication title -
anaesthesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.839
H-Index - 117
eISSN - 1365-2044
pISSN - 0003-2409
DOI - 10.1111/j.1365-2044.2012.07336.x
Subject(s) - propofol , hypoxia (environmental) , catalase , medicine , antioxidant , lactate dehydrogenase , pharmacology , hydrogen peroxide , reactive oxygen species , anesthesia , oxygen , oxidative stress , biochemistry , biology , chemistry , enzyme , organic chemistry
Summary Propofol may protect neuronal cells from hypoxia re‐oxygenation injury, possibly via an antioxidant actions under hypoxic conditions. This study investigated the molecular effects of propofol on hypoxia‐induced cell damage using a neuronal cell line. Cultured human IMR‐32 cells were exposed to propofol (30 μ m ) and biochemical and molecular approaches were used to assess cellular effects. Propofol significantly reduced hypoxia‐mediated increases in lactate dehydrogenase, a marker of cell damage (mean (SD) for normoxia: 0.39 (0.07) a.u.; hypoxia: 0.78 (0.21) a.u.; hypoxia + propofol: 0.44 (0.17) a.u.; normoxia vs hypoxia, p < 0.05; hypoxia vs hypoxia + propofol, p < 0.05), reactive oxygen species and hydrogen peroxide. Propofol also diminished the morphological signs of cell damage. Increased amounts of catalase, which degrades hydrogen peroxide, were detected under hypoxic conditions. Propofol decreased the amount of catalase produced, but increased its enzymatic activity. Propofol protects neuronal cells from hypoxia re‐oxygenation injury, possibly via a combined direct antioxidant effect along with induced cellular antioxidant mechanisms.