You are viewing a javascript disabled version of the site. Please enable Javascript for this site to function properly.
Go to headerGo to navigationGo to searchGo to contentsGo to footer
In content section. Select this link to jump to navigation

The protective effect of North Schisandra Lignans on vascular endothelial cell oxidation injuries

Issue title: Papers from the 4th International Conference on Biomedical Engineering and Biotechnology (ICBEB2015), 18-21 August 2015, Shanghai, China ``New Paradigms for Biomedical Engineering and Biotechnology''

Article type: Research Article

Authors: Zhang, Ruowena | Wang, Yilinb | Zhu, Dongc | Dong, Fengyingd | Chen, Xie; *

Affiliations: [a] Beihua University Faculty of Medicine, Beihua University, Jilin, China | [b] The First Clinical Medical College, Beijing University of Chinese Medicine, Beijing, China | [c] The Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China | [d] Jilin Gynecology and Obstetrics Hospital, Jilin, China | [e] Pathogen Biology Department, College of Basic Medicine, Beihua University, Jilin, China

Correspondence: [*] Corresponding author: Xi Chen, Pathogen Biology Department, College of Basic Medicine, Beihua University, Jilin, China. E-mail:[email protected]

Keywords: North Schisandra Lignans, vascular endothelial cell, superoxide dismutase, malondialdehyde

DOI: 10.3233/THC-161192

Journal: Technology and Health Care, vol. 24, no. s2, pp. S651-S657, 2016

Published: 13 June 2016
Get PDF open access

Abstract

BACKGROUND:

In this study, the authors cultivated ECV-304 in vitro and incubated cells with H2O2, established injury models, and induced oxidized endothelial cell apoptosis. This model makes it possible to choose suitable concentrations of North Schisandra Lignans.

OBJECTIVE:

To study the protective effects of North Schisandra Lignans on human umbilical vein endothelial cell injuries.

METHODS:

Endothelial cell growth and proliferation activity were detected through the MTT method. The colorimetric method was used to determine superoxide dismutase (SOD) activity in the cell culture solution, as well as malondialdehyde (MDA) content in the cell.

RESULTS:

North Schisandra Lignans noticeably decreased ECV-304 cell injury induced by H2O2. Moderate and high concentrations of North Schisandra Lignans could significantly lower MDA content and heighten SOD activity. These differences were significant compared to the H2O2 group (P< 0.05).

CONCLUSIONS:

North Schisandra Lignans had an obvious protective effect on ECV-304 injured by H2O2$. The mechanism decreases MDA production and heightened SOD activity.

References

[1] 

Shimbo D, , Muntner P, , Mann D, et al. Endothelial dysfunction and the risk of hypertension: the multi-ethnic study of atherosclerosis.[J]. Hypertension, (2010) ; 55: (5): 1210-1216.

[2] 

Briasoulis A, , Tousoulis D, , Androulakis ES, et al. Endothelial dysfunction and atherosclerosis: focus on novel therapeutic approaches.[J]. Recent Pat Cardiovasc Drug Discov, (2012) ; 7: (1): 21-32.

[3] 

Liu ZY, , Kong W. The role of adventitia in atherosclerosis.[J]. Sheng Li Ke Xue Jin Zhan, (2010) ; 41: (3): 177-182.

[4] 

Rapezzi C, , Gallo P. Atherosclerosis: A polidistrectual disease.[J]. G Ital Cardiol (Rome), (2010) ; 11: (12 Suppl 3): 43S-48S.

[5] 

Albiero M, , Menegazzo L, , Fadini GP. Circulating smooth muscle progenitors and atherosclerosis.[J]. Trends Cardiovasc Med, (2010) ; 20: (4): 133-140.

[6] 

Filip M, , Maciag J, , Nosalski R, et al. Endothelial dysfunction related to oxidative stress and inflammation in perivascular adipose tissue.[J]. Postepy Biochem, (2012) ; 58: (2): 186-94.

[7] 

Mudau M, , Genis A, et al. Endothelial dysfunction; the early predictor of atherosclerosis.[J]. Cardiovasc J Afr, (2012) ; 23: (4): 222-31.

[8] 

Davignon J, , Ganz P. Role of endothelial dysfunction in atherosclerosis.[J]. Circulation, (2004) ; 109: (23 Suppl 1): III27-32.

[9] 

Lakshmi SV, , Padmaja G, et al. Oxidative stress in cardiovascular disease.[J]. Indian J Biochem Biophys, (2009) ; 46: (6): 421-40.

[10] 

Park JQ, , Oh GT. The role of peroxidases in the pathogenesis of atherosclerosis.[J]. BMB Rep, (2011) ; 44: (8): 497-505.

[11] 

Gao S, , Liu Z, , Li H, et al. Cardiovascular actions and therapeutic potentialof tanshinone IIA.[J]. Atherosclerosis, (2012) ; 220: (1): 3-10.

[12] 

Davignon J, , Ganz P. Role of endothelial dysfunction in atherosclerosis.[J]. Circulation, (2004) ; 109: (23 Suppl 1): III27-32.

[13] 

Karatzis EN. The role of inflammatory agents in endothelial function and their contribution to atherosclerosis.[J]. Hellenic J Cardiol, (2005) ; 46: : 232-239.

[14] 

Vita JA. Endothelial function and clinical outcome.[J]. Heart, (2005) ; 91: : 1278-279.

[15] 

Higashi Y, , Noma K, et al. Endothelial Function and Oxidative Stress in Cardiovascular Diseases.[J]. Circ J, (2009) ; 73: : 411-418.

[16] 

Stirban A. The role of AGEs and ROS in atherosclerosis.[J]. Herz, (2010) ; 35: (3): 170-180.

[17] 

J Biol Chem, (2011) ; 286: (41): 36011-9. doi: 10.1074/jbc.M111.265082. Epub 2011 Aug 24.

[18] 

J Biol Chem, (2013) ; 288: (17): 11940-8. doi: 10.1074/jbc.M112.427674. Epub 2013 Mar 18.

Show more