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Conference Paper: Mechanisms of action of xinmailong, a Chinese medicine derived from periplaneta Americana, in treating heart failure
Title | Mechanisms of action of xinmailong, a Chinese medicine derived from periplaneta Americana, in treating heart failure |
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Authors | |
Keywords | Pharmacy and pharmacology environmental studies Toxicology and environmental safety |
Issue Date | 2014 |
Publisher | Blackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTO |
Citation | The 17th World Congress of Basic and Clinical Pharmacology (WCP2014), Cape Town, South Africa, 13-18 July 2014. In Basic & Clinical Pharmacology & Toxicology, 2014, v. 115 suppl. s1, p. 36, abstract no. 117 How to Cite? |
Abstract | Chronic heart failure is one of the commonest fatal diseases in the world. Much work has been carried out to reveal its complicated pathogenesis and develop effective therapy. Positive inotropic drugs are the major type of drugs used in the treatment of heart failure. Xinmailong is a medicine derived from the extract of Periplaneta Americana. It is marketed in Mainland China as a proprietary product for treating chronic heart failure. Although clinical studies have demonstrated the therapeutic effectiveness of Xinmailong, the mechanism by which it can cure heart failure is still largely unknown. In our study, the results of calcium imaging demonstrated that Xinmailong increased the intracellular calcium level in H9c2, a rat cardiomyoblast cell line, induced by electrical stimulation. Unlike KB-R7943, which is a sodium-calcium exchanger inhibitor, Xinmailong did not affect the basal intracellular calcium level in H9c2 in the absence of electrical stimulation. It, implied that Xinmailong did not work on sodium-calcium exchanger. Xinmailong had no effect of thapsigargin-induced calcium release from sarcoplasmic reticulum. The effect of Xinmailong on intracellular calcium level in H9c2 was not inhibited by nimodipine, which is a L-type calcium channel blocker. It indicated that Xinmailong did not interact with L-type calcium channels. Further study is required to find out how Xinmailong increases intracellular calcium in cardiomyocytes. Apart from the above results, our study also demonstrated that Xinmailong exerted cardioprotective effect by reducing intracellular reactive oxygen species. The mechanism may involve the increased expressions of antioxidant enzymes such as superoxide dismutase 1 and 2. |
Description | Session - Cardiovascular Pharmacology This journal suppl. entitled: Special Issue: Abstracts of the 17th World Congress of Basic and Clinical Pharmacology ... 2014 |
Persistent Identifier | http://hdl.handle.net/10722/204448 |
ISSN | 2023 Impact Factor: 2.7 2023 SCImago Journal Rankings: 0.744 |
DC Field | Value | Language |
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dc.contributor.author | Cheung, C | en_US |
dc.date.accessioned | 2014-09-19T23:52:21Z | - |
dc.date.available | 2014-09-19T23:52:21Z | - |
dc.date.issued | 2014 | en_US |
dc.identifier.citation | The 17th World Congress of Basic and Clinical Pharmacology (WCP2014), Cape Town, South Africa, 13-18 July 2014. In Basic & Clinical Pharmacology & Toxicology, 2014, v. 115 suppl. s1, p. 36, abstract no. 117 | en_US |
dc.identifier.issn | 1742-7835 | - |
dc.identifier.uri | http://hdl.handle.net/10722/204448 | - |
dc.description | Session - Cardiovascular Pharmacology | - |
dc.description | This journal suppl. entitled: Special Issue: Abstracts of the 17th World Congress of Basic and Clinical Pharmacology ... 2014 | - |
dc.description.abstract | Chronic heart failure is one of the commonest fatal diseases in the world. Much work has been carried out to reveal its complicated pathogenesis and develop effective therapy. Positive inotropic drugs are the major type of drugs used in the treatment of heart failure. Xinmailong is a medicine derived from the extract of Periplaneta Americana. It is marketed in Mainland China as a proprietary product for treating chronic heart failure. Although clinical studies have demonstrated the therapeutic effectiveness of Xinmailong, the mechanism by which it can cure heart failure is still largely unknown. In our study, the results of calcium imaging demonstrated that Xinmailong increased the intracellular calcium level in H9c2, a rat cardiomyoblast cell line, induced by electrical stimulation. Unlike KB-R7943, which is a sodium-calcium exchanger inhibitor, Xinmailong did not affect the basal intracellular calcium level in H9c2 in the absence of electrical stimulation. It, implied that Xinmailong did not work on sodium-calcium exchanger. Xinmailong had no effect of thapsigargin-induced calcium release from sarcoplasmic reticulum. The effect of Xinmailong on intracellular calcium level in H9c2 was not inhibited by nimodipine, which is a L-type calcium channel blocker. It indicated that Xinmailong did not interact with L-type calcium channels. Further study is required to find out how Xinmailong increases intracellular calcium in cardiomyocytes. Apart from the above results, our study also demonstrated that Xinmailong exerted cardioprotective effect by reducing intracellular reactive oxygen species. The mechanism may involve the increased expressions of antioxidant enzymes such as superoxide dismutase 1 and 2. | - |
dc.language | eng | en_US |
dc.publisher | Blackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTO | - |
dc.relation.ispartof | Basic & Clinical Pharmacology & Toxicology | en_US |
dc.rights | The definitive version is available at www.blackwell-synergy.com | - |
dc.subject | Pharmacy and pharmacology environmental studies | - |
dc.subject | Toxicology and environmental safety | - |
dc.title | Mechanisms of action of xinmailong, a Chinese medicine derived from periplaneta Americana, in treating heart failure | en_US |
dc.type | Conference_Paper | en_US |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1111/bcpt.12259_1 | - |
dc.identifier.hkuros | 234167 | en_US |
dc.identifier.hkuros | 238804 | - |
dc.identifier.volume | 115 | - |
dc.identifier.issue | suppl. s1 | - |
dc.identifier.spage | 36, abstract no. 117 | - |
dc.identifier.epage | 36, abstract no. 117 | - |
dc.publisher.place | United Kingdom | - |
dc.identifier.issnl | 1742-7835 | - |