Palmatine from Coptidis rhizoma reduces ischemia-reperfusion-mediated acute myocardial injury in the rat
- Authors
- Kim, Young Min; Ha, Yu Mi; Jin, Yong Chun; Shi, Lian Yu; Lee, Yong Soo; Kim, Hye Jung; Seo, Han Geuk; Choi, Jae Soo; Kim, Yeong Shik; Kang, Sam Sik; Lee, Jae Heun; Chang, Ki Churl
- Issue Date
- Aug-2009
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- Ischemia reperfusion injury; Palmatine; Antioxidant action; Oxidative stress
- Citation
- FOOD AND CHEMICAL TOXICOLOGY, v.47, no.8, pp.2097 - 2102
- Indexed
- SCIE
SCOPUS
- Journal Title
- FOOD AND CHEMICAL TOXICOLOGY
- Volume
- 47
- Number
- 8
- Start Page
- 2097
- End Page
- 2102
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/26215
- DOI
- 10.1016/j.fct.2009.05.031
- ISSN
- 0278-6915
- Abstract
- The aim of the present study was to evaluate the protective effect of palmatine, one of active ingredients of Coptidis rhizoma, against myocardial ischemia-reperfusion (I/R) injury is due to its antioxidant and anti-inflammatory action. Adult male rats were subjected to 30 min of ischemia and 6 or 24 h of reperfusion. Rats were randomized to receive vehicle or palmatine 1 h before reperfusion. Infarct size, myocardial function, and the antioxidant enzyme activity, such as malonaldehyde (MDA), lactate dehydrogenase (LDH), creatine phosphokinase (CK), superoxide dismutase (SOD) and catalase (CAT) were measured. Palmatine significantly improved I/R-induced myocardial dysfunction by increasing the values of the first derivative (+/- dp/dt) of left ventricular pressure and decreased infarct size by 50% (P < 0.01 versus vehicle). As expected, palmatine markedly inhibited the increase of LDH, CK, and MDA contents in I/R rat serum, and it also significantly inhibited the decline of the activity of SOD and CAT in I/R cardiac tissues. In addition, COX-2 and NOS expression in I/R myocardium was significantly reduced. Interestingly, plamatine increased heme oxygenase (HO)-1 induction in human aortic endothelial cells. We concluded that palmatine protects hearts from I/R injury in rats possibly by reducing oxidative stress and modulating inflammatory mediators. (C) 2009 Elsevier Ltd. All rights reserved.
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