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Clematichinenoside attenuates myocardial infarction in ischemia/reperfusion injury both in vivo and in vitro.
Planta Med. 2013 Sep; 79(14):1289-97.PM

Abstract

Clematichinenoside is a triterpenoid saponin isolated from the roots of Clematis chinensis. Oxidative stress and excessive nitric oxide production are thought to play considerable roles in ischemia/reperfusion injury that impairs cardiac function. The present study investigated the protective effect of clematichinenoside on regional and global ischemia/reperfusion injury and ventricular myocytes. In vivo, regional myocardial ischemia/reperfusion injury of rats was induced by the occlusion of the left anterior descending coronary artery, and isolated guinea pigs heart using Langendorff apparatus served as a global ischemia/reperfusion injury model ex vivo. Primary cultured neonatal ventricular myocytes were further applied to explore the anti-ischemia/reperfusion injury property in vitro. Infarct size was measured with TTC stain; enzyme activities such as lactate dehydrogenase, creatine kinase, superoxide dismutase, malondialdehyde, and nitric oxide were analyzed with assay kits; inducible nitric oxide synthase and endothelial nitric oxide synthase expressions were determined by Western blot. Clematichinenoside attenuated infarct size, decreased lactate dehydrogenase, creatine kinase, and malondialdehyde levels and enhanced superoxide dismutase activity. Clematichinenoside improved hemodynamics indexes, such as left ventricular developed pressure, maximum left ventricular developed pressure, and increase/decrease rate (± dp/dtmax) in the isolated guinea pig heart after reperfusion. Clematichinenoside also inhibited excessive production of nitric oxide through downregulating inducible nitric oxide synthase as well as upregulating endothelial nitric oxide synthase during ischemia/reperfusion injury. Clematichinenoside attenuates ischemia/reperfusion injury in vivo, ex vivo, and in vitro via an antioxidant effect and by restoring the balance between inducible nitric oxide synthase and endothelial nitric oxide synthase.

Authors+Show Affiliations

State Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, Nanjing, P. R. China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23929248

Citation

Zhang, Rui, et al. "Clematichinenoside Attenuates Myocardial Infarction in Ischemia/reperfusion Injury Both in Vivo and in Vitro." Planta Medica, vol. 79, no. 14, 2013, pp. 1289-97.
Zhang R, Fang W, Han D, et al. Clematichinenoside attenuates myocardial infarction in ischemia/reperfusion injury both in vivo and in vitro. Planta Med. 2013;79(14):1289-97.
Zhang, R., Fang, W., Han, D., Sha, L., Wei, J., Liu, L., & Li, Y. (2013). Clematichinenoside attenuates myocardial infarction in ischemia/reperfusion injury both in vivo and in vitro. Planta Medica, 79(14), 1289-97. https://doi.org/10.1055/s-0033-1350671
Zhang R, et al. Clematichinenoside Attenuates Myocardial Infarction in Ischemia/reperfusion Injury Both in Vivo and in Vitro. Planta Med. 2013;79(14):1289-97. PubMed PMID: 23929248.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Clematichinenoside attenuates myocardial infarction in ischemia/reperfusion injury both in vivo and in vitro. AU - Zhang,Rui, AU - Fang,Weirong, AU - Han,Dan, AU - Sha,Lan, AU - Wei,Jie, AU - Liu,Lifang, AU - Li,Yunman, Y1 - 2013/08/08/ PY - 2013/8/10/entrez PY - 2013/8/10/pubmed PY - 2014/4/9/medline SP - 1289 EP - 97 JF - Planta medica JO - Planta Med. VL - 79 IS - 14 N2 - Clematichinenoside is a triterpenoid saponin isolated from the roots of Clematis chinensis. Oxidative stress and excessive nitric oxide production are thought to play considerable roles in ischemia/reperfusion injury that impairs cardiac function. The present study investigated the protective effect of clematichinenoside on regional and global ischemia/reperfusion injury and ventricular myocytes. In vivo, regional myocardial ischemia/reperfusion injury of rats was induced by the occlusion of the left anterior descending coronary artery, and isolated guinea pigs heart using Langendorff apparatus served as a global ischemia/reperfusion injury model ex vivo. Primary cultured neonatal ventricular myocytes were further applied to explore the anti-ischemia/reperfusion injury property in vitro. Infarct size was measured with TTC stain; enzyme activities such as lactate dehydrogenase, creatine kinase, superoxide dismutase, malondialdehyde, and nitric oxide were analyzed with assay kits; inducible nitric oxide synthase and endothelial nitric oxide synthase expressions were determined by Western blot. Clematichinenoside attenuated infarct size, decreased lactate dehydrogenase, creatine kinase, and malondialdehyde levels and enhanced superoxide dismutase activity. Clematichinenoside improved hemodynamics indexes, such as left ventricular developed pressure, maximum left ventricular developed pressure, and increase/decrease rate (± dp/dtmax) in the isolated guinea pig heart after reperfusion. Clematichinenoside also inhibited excessive production of nitric oxide through downregulating inducible nitric oxide synthase as well as upregulating endothelial nitric oxide synthase during ischemia/reperfusion injury. Clematichinenoside attenuates ischemia/reperfusion injury in vivo, ex vivo, and in vitro via an antioxidant effect and by restoring the balance between inducible nitric oxide synthase and endothelial nitric oxide synthase. SN - 1439-0221 UR - https://www.unboundmedicine.com/medline/citation/23929248/Clematichinenoside_attenuates_myocardial_infarction_in_ischemia/reperfusion_injury_both_in_vivo_and_in_vitro_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1055/s-0033-1350671 DB - PRIME DP - Unbound Medicine ER -