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Anesth Analg 2008; 107:534-540
© 2008 International Anesthesia Research Society
doi: 10.1213/ane.0b013e3181770be9
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ANESTHETIC PHARMACOLOGY

Propofol Protects Hepatic L02 Cells from Hydrogen Peroxide-Induced Apoptosis via Activation of Extracellular Signal-Regulated Kinases Pathway

Hao Wang, MD, PhD*, Zhanggang Xue, MD*, Qiong Wang, MS{dagger}, Xiaochen Feng, MS{dagger}, and Zonghou Shen, PhD{dagger}

From the *Department of Anesthesiology, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China; and {dagger}Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, People’s Republic of China.

Address correspondence and reprint requests to Zhanggang Xue, MD, Department of Anesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, People’s. Republic of China. Address e-mail to zhanggangxue{at}gmail.com.

BACKGROUND: Propofol protects cells against ischemia/reperfusion injury in several organs, but there are few reports of its effect on liver epithelial cells. We investigated the effect of propofol preconditioning on human hepatic L02 cells under hydrogen peroxide (H2O2)-induced oxidative stress and attempted to determine whether the extracellular signal-regulated kinases (ERK) pathway is involved in this process.

METHODS: Preconditioned or nonpreconditioned human hepatic L02 cells were exposed to H2O2 and the changes of apoptosis were evaluated by TUNEL assay, Caspase-3 and poly ADP-ribose polymerase (PARP) cleavage. Activation of ERK1/2 and mitogen-activated protein kinase//ERK Kinase 1/2 (MEK1/2) was measured by Western blot analysis. The mRNA expression of Bcl-2, Bcl-xL, Bad, and Bax was quantified by real-time quantitative reverse transcriptase polymerase chain reaction.

RESULTS: Propofol preconditioning reduced the population of apoptotic cells and Caspase-3 and PARP cleavage induced by H2O2 inhepatic L02 cells. L02 cells treated with propofol (0.01–0.3 mM) alone, led to a dose-dependent activation of ERK and MEK, and such activation was detected within 0.5 h and eventually declined to <50% at 4 h. The addition of the specific inhibitor PD98059 completely abolished the activation of ERK and aggravated the extent of apoptosis. Moreover, propofol treatment repressed the mRNA expression of proapoptotic genes Bad and Bax, and this repression could be partly reversed by PD98059.

CONCLUSIONS: These findings demonstrate that propofol protects hepatic L02 cells from H2O2-induced apoptosis, partly through activating the MEK-ERK pathway and further suppressing Bad and Bax expression.






Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2008 by the International Anesthesia Research Society.