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Published in: Inflammation 4/2015

01-08-2015

Effects of Salidroside on Myocardial Injury In Vivo In Vitro via Regulation of Nox/NF-κB/AP1 Pathway

Authors: Lingpeng Zhu, Tingting Wei, Xiayun Chang, He He, Jin Gao, Zhengli Wen, Tianhua Yan

Published in: Inflammation | Issue 4/2015

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Abstract

Salidroside (Sal), a phenylpropanoid glycoside isolated from a popular traditional Chinese medicinal plant Rhodiola rosea L., possesses multiple pharmacological actions. This aim of this study is to investigate the effects of Sal against isoproterenol (ISO)-induced myocardial ischemia. Fifty male Sprague–Dawley rats were randomized equally to five groups: control group, ISO group, Sal (20 mg/kg; 40 mg/kg) treatments groups, and propranolol (Pro, 15 mg/kg) group. Rats were treated for 14 days and then given ISO (80 mg/kg) for 2 consecutive days by subcutaneous injection. In vitro, we used H9C2 cells to investigate the effects of Sal against hypoxia–reoxygenation. ST-segment elevation was measured after the last administration. Serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD), and malondialdehyde (MDA); levels of NADPH oxidases 2 and 4 (Nox2 and Nox4), NF-κBP65, and AP1 in heart, and H9C2 cells were measured by Western blot. The hearts were excised for determining microscopic examination, SOD, and MDA measurements. Sal decreased the ST elevation induced by ISO, decreased serum levels of CK-MB, LDH, TNF-α, IL-6, SOD, and MDA. In addition, Sal increased SOD activity and decreased MDA content in myocardial tissue. Sal also decreased Nox2 and 4, NF-κBP65, P-NF-κBP65, and AP1 protein levels in the heart. The results support a further study of Sal as potential treatments for ischemic heart disease.
Literature
1.
go back to reference Lopez, A.D., C.D. Mathers, M. Ezzati, D.T. Jamison, and C.J.L. Murray. 2006. Global burden of disease and risk factors. Washington (DC): World Bank.CrossRef Lopez, A.D., C.D. Mathers, M. Ezzati, D.T. Jamison, and C.J.L. Murray. 2006. Global burden of disease and risk factors. Washington (DC): World Bank.CrossRef
2.
go back to reference Yang, G., Y. Wang, Y. Zeng, G.F. Gao, X. Liang, M. Zhou, X. Wan, S. Yu, Y. Jiang, M. Naqhavi, T. Vos, H. Wang, A.D. Lopez, and C.J. Murray. 2013. Rapid health transition in China, 1990–2010: findings from the Global Burden of Disease Study 2010. Lancet 381: 1987–2015.PubMedCrossRef Yang, G., Y. Wang, Y. Zeng, G.F. Gao, X. Liang, M. Zhou, X. Wan, S. Yu, Y. Jiang, M. Naqhavi, T. Vos, H. Wang, A.D. Lopez, and C.J. Murray. 2013. Rapid health transition in China, 1990–2010: findings from the Global Burden of Disease Study 2010. Lancet 381: 1987–2015.PubMedCrossRef
3.
go back to reference Griendling, K.K., D. Sorescu, and M. Ushio-Fukai. 2000. NAD(P)H oxidase role in cardiovascular biology and disease. Circulation Research 86: 494–501.PubMedCrossRef Griendling, K.K., D. Sorescu, and M. Ushio-Fukai. 2000. NAD(P)H oxidase role in cardiovascular biology and disease. Circulation Research 86: 494–501.PubMedCrossRef
4.
go back to reference Guha, M., W. Bai, J.L. Nadler, et al. 2000. Molecular mechanisms of tumor necrosis factor alpha gene expression in monocytic cells via hyperglycemia-induced oxidant stress-dependent and -independent pathways. Journal of Biological Chemistry 275: 17728e39.CrossRef Guha, M., W. Bai, J.L. Nadler, et al. 2000. Molecular mechanisms of tumor necrosis factor alpha gene expression in monocytic cells via hyperglycemia-induced oxidant stress-dependent and -independent pathways. Journal of Biological Chemistry 275: 17728e39.CrossRef
5.
go back to reference Schreck, R., K. Albermann, and P.A. Baeuerle. 1992. Nuclear factor kappa B: an oxidative stress-responsive transcription factor of eukaryotic cells (a review). Free Radical Research Communications 17: 221e37. Schreck, R., K. Albermann, and P.A. Baeuerle. 1992. Nuclear factor kappa B: an oxidative stress-responsive transcription factor of eukaryotic cells (a review). Free Radical Research Communications 17: 221e37.
6.
go back to reference Kucinskaite, A., V. Briedis, and A. Savickas. 2004. Experimental analysis of therapeutic properties of Rhodiola rosea L and its possible application in medicine. Medicina (Kaunas, Lithuania) 40: 614–619. Kucinskaite, A., V. Briedis, and A. Savickas. 2004. Experimental analysis of therapeutic properties of Rhodiola rosea L and its possible application in medicine. Medicina (Kaunas, Lithuania) 40: 614–619.
7.
go back to reference Willerson, J.T., and P.M. Ridker. 2004. Inflammation as a cardiovascular risk factor. Circulation 109: II2–10.PubMedCrossRef Willerson, J.T., and P.M. Ridker. 2004. Inflammation as a cardiovascular risk factor. Circulation 109: II2–10.PubMedCrossRef
8.
go back to reference Zheng, W., L.Z. Huang, L. Zhao, B. Wang, H.B. Xu, G.Y. Wang, Z.L. Wang, and H. Zhou. 2008. Superoxide dismutase activity and malondialdehyde level in plasma and morphological evaluation of acute severe hemorrhagic shock in rats. American Journal of Emergency Medicine 26: 54–58.PubMedCrossRef Zheng, W., L.Z. Huang, L. Zhao, B. Wang, H.B. Xu, G.Y. Wang, Z.L. Wang, and H. Zhou. 2008. Superoxide dismutase activity and malondialdehyde level in plasma and morphological evaluation of acute severe hemorrhagic shock in rats. American Journal of Emergency Medicine 26: 54–58.PubMedCrossRef
9.
go back to reference Senthil, S., G. Chandramohan, and K.V. Pugalendi. 2007. Isomers (oleanolic and ursolic acids) differ in their protective effect against isoproterenol-induced myocardial ischemia in rats. International Journal of Cardiology 119: 131–133.PubMedCrossRef Senthil, S., G. Chandramohan, and K.V. Pugalendi. 2007. Isomers (oleanolic and ursolic acids) differ in their protective effect against isoproterenol-induced myocardial ischemia in rats. International Journal of Cardiology 119: 131–133.PubMedCrossRef
Metadata
Title
Effects of Salidroside on Myocardial Injury In Vivo In Vitro via Regulation of Nox/NF-κB/AP1 Pathway
Authors
Lingpeng Zhu
Tingting Wei
Xiayun Chang
He He
Jin Gao
Zhengli Wen
Tianhua Yan
Publication date
01-08-2015
Publisher
Springer US
Published in
Inflammation / Issue 4/2015
Print ISSN: 0360-3997
Electronic ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-015-0134-0

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