Source:http://linkedlifedata.com/resource/pubmed/id/18048101
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
umls-concept:C0022116,
umls-concept:C0035124,
umls-concept:C0175677,
umls-concept:C0178784,
umls-concept:C0205198,
umls-concept:C0242726,
umls-concept:C0696940,
umls-concept:C1280500,
umls-concept:C1441547,
umls-concept:C1521840,
umls-concept:C1555707,
umls-concept:C1705851,
umls-concept:C2699787,
umls-concept:C2752151,
umls-concept:C2828366
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| pubmed:issue |
2
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| pubmed:dateCreated |
2008-1-28
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| pubmed:abstractText |
Ischemia and reperfusion (I/R) exerts multiple insults in microcirculation, frequently accompanied by endothelial cell injury, enhanced adhesion of leukocytes, macromolecular efflux, production of oxygen free radicals, and mast cell degranulation. Since the microcirculatory disturbance results in injury of organ involved, protection of organ after I/R is of great importance in clinic. Salvia miltiorrhiza root has long been used in Asian countries for clinical treatment of various microcirculatory disturbance-related diseases. This herbal drug contains many active water-soluble compounds, including protocatechuic aldehyde (PAl), 3,4-dihydroxyphenyl lactic acid (DLA) and salvianolic acid B (SalB). These compounds, as well as water-soluble fraction of S. miltiorrhiza root extract (SMRE), have an ability to scavenge peroxides and are able to inhibit the expression of adhesion molecules in vascular endothelium and leukocytes. Moreover, lipophilic compounds of SMRE also prevent the development of vascular damage; NADPH oxidase and platelet aggregation are inhibited by tanshinone IIA and tanshinone IIB, respectively, and the mast cell degranulation is blunted by cryptotanshinone and 15,16-dihydrotanshinone I. Thus, the water-soluble and lipophilic compounds of SMRE appear to improve the I/R-induced vascular damage multifactorially and synergically. This review will summarize the ameliorating effect of compounds derived from SMRE on microcirculatory disturbance and target organ injury after I/R and will provide a new perspective on remedy with multiple drugs.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0163-7258
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
117
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
280-95
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:18048101-Animals,
pubmed-meshheading:18048101-Blood Platelets,
pubmed-meshheading:18048101-Brain,
pubmed-meshheading:18048101-Cardiovascular Agents,
pubmed-meshheading:18048101-Cell Degranulation,
pubmed-meshheading:18048101-Cerebrovascular Circulation,
pubmed-meshheading:18048101-Coronary Circulation,
pubmed-meshheading:18048101-Cytokines,
pubmed-meshheading:18048101-Drugs, Chinese Herbal,
pubmed-meshheading:18048101-Endothelial Cells,
pubmed-meshheading:18048101-Humans,
pubmed-meshheading:18048101-Kidney,
pubmed-meshheading:18048101-Leukocytes,
pubmed-meshheading:18048101-Liver,
pubmed-meshheading:18048101-Liver Circulation,
pubmed-meshheading:18048101-Lung,
pubmed-meshheading:18048101-Mast Cells,
pubmed-meshheading:18048101-Microcirculation,
pubmed-meshheading:18048101-Molecular Structure,
pubmed-meshheading:18048101-Myocardial Reperfusion Injury,
pubmed-meshheading:18048101-Plant Extracts,
pubmed-meshheading:18048101-Plant Roots,
pubmed-meshheading:18048101-Renal Circulation,
pubmed-meshheading:18048101-Reperfusion Injury,
pubmed-meshheading:18048101-Salvia miltiorrhiza
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| pubmed:year |
2008
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| pubmed:articleTitle |
Ameliorating effects of compounds derived from Salvia miltiorrhiza root extract on microcirculatory disturbance and target organ injury by ischemia and reperfusion.
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| pubmed:affiliation |
Department of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing, China. kan@chuigaku.co.jp <kan@chuigaku.co.jp>
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| pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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