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Propofol protects hepatic L02 cells from hydrogen peroxide-induced apoptosis via activation of extracellular signal-regulated kinases pathway.
Anesth Analg. 2008 Aug; 107(2):534-40.A&A

Abstract

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-x(L), 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.

Authors+Show Affiliations

Department of Anesthesiology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18633031

Citation

Wang, Hao, et al. "Propofol Protects Hepatic L02 Cells From Hydrogen Peroxide-induced Apoptosis Via Activation of Extracellular Signal-regulated Kinases Pathway." Anesthesia and Analgesia, vol. 107, no. 2, 2008, pp. 534-40.
Wang H, Xue Z, Wang Q, et al. Propofol protects hepatic L02 cells from hydrogen peroxide-induced apoptosis via activation of extracellular signal-regulated kinases pathway. Anesth Analg. 2008;107(2):534-40.
Wang, H., Xue, Z., Wang, Q., Feng, X., & Shen, Z. (2008). Propofol protects hepatic L02 cells from hydrogen peroxide-induced apoptosis via activation of extracellular signal-regulated kinases pathway. Anesthesia and Analgesia, 107(2), 534-40. https://doi.org/10.1213/ane.0b013e3181770be9
Wang H, et al. Propofol Protects Hepatic L02 Cells From Hydrogen Peroxide-induced Apoptosis Via Activation of Extracellular Signal-regulated Kinases Pathway. Anesth Analg. 2008;107(2):534-40. PubMed PMID: 18633031.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Propofol protects hepatic L02 cells from hydrogen peroxide-induced apoptosis via activation of extracellular signal-regulated kinases pathway. AU - Wang,Hao, AU - Xue,Zhanggang, AU - Wang,Qiong, AU - Feng,Xiaochen, AU - Shen,Zonghou, PY - 2008/7/18/pubmed PY - 2008/8/30/medline PY - 2008/7/18/entrez SP - 534 EP - 40 JF - Anesthesia and analgesia JO - Anesth Analg VL - 107 IS - 2 N2 - 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-x(L), 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. SN - 1526-7598 UR - https://www.unboundmedicine.com/medline/citation/18633031/Propofol_protects_hepatic_L02_cells_from_hydrogen_peroxide_induced_apoptosis_via_activation_of_extracellular_signal_regulated_kinases_pathway_ L2 - https://doi.org/10.1213/ane.0b013e3181770be9 DB - PRIME DP - Unbound Medicine ER -