Share This Article:

Protective Effect of Catalpol on Myocardium in Rats with Isoprenaline-Induced Myocardial Infarcts via Angiogenesis through Endothelial Progenitor Cells and Notch1 Signaling Pathway

Abstract Full-Text HTML Download Download as PDF (Size:1172KB) PP. 619-627
DOI: 10.4236/pp.2013.48088    2,503 Downloads   4,005 Views   Citations

ABSTRACT

Protective effect of catalpol on myocardium was studied in relation to endothelial progenitor cells, Notch1 signaling pathway and angiogenesis in rats with isoprenaline (INN)-induced acute myocardial infarcts. To analyze the pathological status and impact of catalpol on the rats, 3 weeks after intragastric gavage, the animals were verified for myocardial infarcts with electrocardiogram and measured for enzyme activity of lactate dehydrogenase (LDH), malondialdehyde (MDA), creatine kinase (CK) and superoxide dismutase (SOD) in myocardium, and further analyzed using HE and TTC staining, as well as visual examination of infarct area. Flow cytometry study of endothelial progenitor cells (EPCs) indicated that the EPCs were mobilized during infarction. The roles of Notch1 signaling pathway in angiogenesis of the infracted animals were studied using immunohistochemistry analysis of RBPjκ and Western blot analysis of Notch1 and Jagged1. Our results obtained from the rats treated with catalpol, positive drug and control showed that catalpol could protect rats from infarction probably by mobilization of EPCs and activation of Notch1 signaling pathway.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

J. Zeng, F. Huang, Y. Tu, S. Wu, M. Li and X. Tong, "Protective Effect of Catalpol on Myocardium in Rats with Isoprenaline-Induced Myocardial Infarcts via Angiogenesis through Endothelial Progenitor Cells and Notch1 Signaling Pathway," Pharmacology & Pharmacy, Vol. 4 No. 8, 2013, pp. 619-627. doi: 10.4236/pp.2013.48088.

References

[1] T. Asahara, T. Murohara, A. Sullivan, et al., “Isolation of Putative Progenitor Endothelial Cells for Angiogenesis,” Science, Vol. 275, No. 5302, 1997, pp. 964-966.
http://dx.doi.org/10.1126/science.275.5302.964
[2] T. Asahara, T. Takahashi, H. Masuda, et al., “VEGF Contributes to Postnatal Neovascularization by Mobilizing Bone Marrow-Derived Endothelial Progenitor Cells,” The EMBO Journal, Vol. 18, No. 14, 1999, pp. 3964-3972.
http://dx.doi.org/10.1093/emboj/18.14.3964
[3] T. Takahashi, C. Kalka, H. Masuda, et al., “Ischemia-and Cytokine-Induced Mobilization of Bone Marrow-Derived Endothelial Progenitor Cells for Neovascularization,” Nature Medicine, Vol. 5, No. 4, 1999, pp. 434-438.
http://dx.doi.org/10.1038/7434
[4] T. Gridley, “Notch Signaling in Vertebrate Development and Disease,” Molecular and Cellular Neuroscience, Vol. 9, No. 2, 1997, pp. 103-108.
http://dx.doi.org/10.1006/mcne.1997.0610
[5] L. T. Krebs, Y. Xue, C. R. Norton, et al., “Notch Signaling Is Essential for Vascular Morphogenesis in Mice,” Genes & Development, Vol. 14, No. 11, 2000, pp. 1343-1352.
[6] Y. Xue, X. Gao, C. E. Lindsell, et al., “Embryonic Lethality and Vascular Defects in Mice Lacking the Notch Ligand Jagged1,” Human Molecular Genetics, Vol. 8, No. 5, 1999, pp. 723-730.
http://dx.doi.org/10.1093/hmg/8.5.723
[7] S.-M. Kwon, M. Eguchi, M. Wada, et al., “Specific Jagged-1 Signal from Bone Marrow Microenvironment Is Required for Endothelial Progenitor Cell Development for Neovascularization,” Circulation, Vol. 118, No. 2, 2008, pp. 157-165.
http://dx.doi.org/10.1161/CIRCULATIONAHA.107.754978
[8] X. Tong, Z. Yang, S. Xian, et al., “Clinical Observation on Mobilization Effect of Bone Marrow Stem Cells with Bushen Huoxue Fonmula in Acute Myocardial Infraction,” Liaoning Journal of Traditional Chinese Medicine, Vol. 37, No. 10, 2010, pp. 1963-1965.
[9] X. Tong, Z. Yang, S. Xian, et al., “Study on Bushen Huoxue Recipe Mobilizing Marrow Stem Cells of Acute Myocadial Infraction in Rats,” Chinese Journal of Basic Medicine in Traditional Chinese Medicine, Vol. 14, No. 8, 2008, pp. 588-591.
[10] D.-Q. Li, Y.-L. Duan, Y.-M. Bao, et al., “Neuroprotection of Catalpol in Transient Global Ischemia in Gerbils,” Neuroscience Research, Vol. 50, No. 2, 2004, pp. 169-177. http://dx.doi.org/10.1016/j.neures.2004.06.009
[11] J. Seng, S. Luo, K. Ma, et al., “Research Advancements for Biomarkers Used in Acute Myocardial Infraction,” Advices in Cardiovascular Diseases, Vol. 33, No. 1, 2012, pp. 106-106.
[12] L. Han and K. Chen, “Injurious Effect of Ischemic Reperfution and the Protective Effect of Yi-Xin-Kang Capsule on Rat Myocardial Mitochondria,” Chinese Journal of Geriatric Cardiovascular and Cerebrovascular Diseases, Vol. 3, No. 5, 2001, pp. 331-332.
[13] E. Mannarino and M. Pirro, “Endothelial Injury and Repair: A Novel Theory for Atherosclerosis,” Angiology, Vol. 59, No. 2, 2008, pp. 69S-72S.
http://dx.doi.org/10.1177/0003319708320761
[14] C. Real, F. Caiado and S. Dias, “Endothelial Progenitors in Vascular Repair and Angiogenesis: How Many Are Needed and What to Do?” Cardiovascular & Haematological Disorders-Drug Targets, Vol. 8, No. 3, 2008, pp. 185-192.
[15] J. Lin, L. Xv, D. Yang, et al., “Effect of Tetramethylpyrazine on the Function of Endothelial Progenitor Cells in Vitro,” Journal of Zhejiang University of Traditional Chinese Medicine, Vol. 32, No. 5, 2008, pp. 598-600.
[16] E. A. Jones, F. le Noble and A. Eichmann, “What Determines Blood Vessel Structure? Genetic Prespecification vs. Hemodynamics,” Physiology, Vol. 21, No. 6, 2006, pp. 388-395. http://dx.doi.org/10.1152/physiol.00020.2006
[17] F. N. Karanu, B. Murdoch, L. Gallacher, et al., “The Notch Ligand Jagged-1 Represents a Novel Growth Factor of Human Hematopoietic Stem Cells,” The Journal of Experimental Medicine, Vol. 192, No. 9, 2000, pp. 1365-1372. http://dx.doi.org/10.1084/jem.192.9.1365

  
comments powered by Disqus

Copyright © 2019 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.