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Catalpol inhibits apoptosis in hydrogen peroxide-induced endothelium by activating the PI3K/Akt signaling pathway and modulating expression of Bcl-2 and Bax.
Eur J Pharmacol. 2010 Feb 25; 628(1-3):155-63.EJ

Abstract

Catalpol, an iridoid glucoside found in the root of Rehmannia glutinosa Libosch, has been demonstrated to reduce apoptosis in neuronal cell lines. Recent data suggests that catalpol also exerts anti-apoptotic effects on other cell types. The aim of the present study was to investigate whether catalpol protects against hydrogen peroxide (H(2)O(2)) induced apoptosis in human umbilical vein endothelial cells (HUVECs). Apoptotic cells were detected by terminal deoxyribonucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling, Annexin V-fluorescein isothiocyanate binding assay and by assessment of caspase-3 activity. The level of intracellular reactive oxygen species was quantified by 2', 7'-dichlorofluorescein diacetate assay. Expression of Akt, Bad, Bcl-2 and Bax mRNA and protein was determined by real-time semiquantitative reverse transcription-polymerase chain reaction and Western blotting. Apoptosis in HUVECs was associated with increased Bax, decreased Bcl-2 activity and inactivated phosphorylation of Akt and Bad after 24h of H(2)O(2) exposure. Pre-treatment of HUVECs with catalpol significantly reduced H(2)O(2)-induced intracellular reactive oxygen species release. Catalpol not only increased the expression of Bcl-2, while decreasing Bax expression, but also induced Akt activation and Bad phosphorylation, and ultimately reduced H(2)O(2)-induced apoptosis. The protective effects of catalpol were partially inhibited by the phosphatidylinositol 3-kinase (PI3K) antagonist wortmannin or 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002). Taken together, these results suggest that pre-treatment of HUVECs with catalpol can block H(2)O(2)-induced apoptosis, and that the underlying mechanism involves reactive oxygen species scavenging, activation of the PI3K/Akt-Bad signaling pathway and increased Bcl-2 and decreased Bax expression.

Authors+Show Affiliations

Department of Cardiology, The First Affiliated Hospital of China Medical University, Liaoning, China.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19962976

Citation

Hu, Lingai, et al. "Catalpol Inhibits Apoptosis in Hydrogen Peroxide-induced Endothelium By Activating the PI3K/Akt Signaling Pathway and Modulating Expression of Bcl-2 and Bax." European Journal of Pharmacology, vol. 628, no. 1-3, 2010, pp. 155-63.
Hu L, Sun Y, Hu J. Catalpol inhibits apoptosis in hydrogen peroxide-induced endothelium by activating the PI3K/Akt signaling pathway and modulating expression of Bcl-2 and Bax. Eur J Pharmacol. 2010;628(1-3):155-63.
Hu, L., Sun, Y., & Hu, J. (2010). Catalpol inhibits apoptosis in hydrogen peroxide-induced endothelium by activating the PI3K/Akt signaling pathway and modulating expression of Bcl-2 and Bax. European Journal of Pharmacology, 628(1-3), 155-63. https://doi.org/10.1016/j.ejphar.2009.11.046
Hu L, Sun Y, Hu J. Catalpol Inhibits Apoptosis in Hydrogen Peroxide-induced Endothelium By Activating the PI3K/Akt Signaling Pathway and Modulating Expression of Bcl-2 and Bax. Eur J Pharmacol. 2010 Feb 25;628(1-3):155-63. PubMed PMID: 19962976.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Catalpol inhibits apoptosis in hydrogen peroxide-induced endothelium by activating the PI3K/Akt signaling pathway and modulating expression of Bcl-2 and Bax. AU - Hu,Lingai, AU - Sun,Yukun, AU - Hu,Jian, Y1 - 2009/12/03/ PY - 2009/05/20/received PY - 2009/11/13/revised PY - 2009/11/23/accepted PY - 2009/12/8/entrez PY - 2009/12/8/pubmed PY - 2010/4/7/medline SP - 155 EP - 63 JF - European journal of pharmacology JO - Eur. J. Pharmacol. VL - 628 IS - 1-3 N2 - Catalpol, an iridoid glucoside found in the root of Rehmannia glutinosa Libosch, has been demonstrated to reduce apoptosis in neuronal cell lines. Recent data suggests that catalpol also exerts anti-apoptotic effects on other cell types. The aim of the present study was to investigate whether catalpol protects against hydrogen peroxide (H(2)O(2)) induced apoptosis in human umbilical vein endothelial cells (HUVECs). Apoptotic cells were detected by terminal deoxyribonucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling, Annexin V-fluorescein isothiocyanate binding assay and by assessment of caspase-3 activity. The level of intracellular reactive oxygen species was quantified by 2', 7'-dichlorofluorescein diacetate assay. Expression of Akt, Bad, Bcl-2 and Bax mRNA and protein was determined by real-time semiquantitative reverse transcription-polymerase chain reaction and Western blotting. Apoptosis in HUVECs was associated with increased Bax, decreased Bcl-2 activity and inactivated phosphorylation of Akt and Bad after 24h of H(2)O(2) exposure. Pre-treatment of HUVECs with catalpol significantly reduced H(2)O(2)-induced intracellular reactive oxygen species release. Catalpol not only increased the expression of Bcl-2, while decreasing Bax expression, but also induced Akt activation and Bad phosphorylation, and ultimately reduced H(2)O(2)-induced apoptosis. The protective effects of catalpol were partially inhibited by the phosphatidylinositol 3-kinase (PI3K) antagonist wortmannin or 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002). Taken together, these results suggest that pre-treatment of HUVECs with catalpol can block H(2)O(2)-induced apoptosis, and that the underlying mechanism involves reactive oxygen species scavenging, activation of the PI3K/Akt-Bad signaling pathway and increased Bcl-2 and decreased Bax expression. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/19962976/Catalpol_inhibits_apoptosis_in_hydrogen_peroxide_induced_endothelium_by_activating_the_PI3K/Akt_signaling_pathway_and_modulating_expression_of_Bcl_2_and_Bax_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(09)01098-X DB - PRIME DP - Unbound Medicine ER -