Protective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats.
<h4>Background</h4>Our previous studies suggested that deoxyschizandrin (DSD) and schisantherin A (STA) may have cardioprotective effects, but information in this regard is lacking. Therefore, we explored the protective role of DSD and STA in myocardial ischemia-reperfusion (I/R) injury....
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oai:doaj.org-article:f7934d4ad92a48119553113c5692b9a42021-11-18T07:48:44ZProtective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats.1932-620310.1371/journal.pone.0061590https://doaj.org/article/f7934d4ad92a48119553113c5692b9a42013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23620773/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Our previous studies suggested that deoxyschizandrin (DSD) and schisantherin A (STA) may have cardioprotective effects, but information in this regard is lacking. Therefore, we explored the protective role of DSD and STA in myocardial ischemia-reperfusion (I/R) injury.<h4>Methodology/principal findings</h4>Anesthetized male rats were treated once with DSD and STA (each 40 µmol/kg) through the tail vein after 45 min of ischemia, followed by 2-h reperfusion. Cardiac function, infarct size, biochemical markers, histopathology and apoptosis were measured and mRNA expression of gp91 (phox) in myocardial tissue assessed by RT-PCR. Neonatal rat cardiomyocytes were pretreated with DSD and STA and then damaged by H2O2. Cell apoptosis was tested by a flow cytometric assay. Compared with the I/R group: (i) DSD and STA could significantly reduce the abnormalities of LVSP, LVEDP, ±dp/dtmax and arrhythmias, thereby showing their protective roles in cardiac function; (ii) DSD and STA could significantly attenuate the infarct size and MDA release while increasing SOD activity, suggesting a role in reducing myocardial injury; (iii) tissue morphology and myocardial textual analysis revealed that DSD and STA mitigated changes in myocardial histopathology; (iv) DSD and STA decreased apoptosis (33.56±2.58% to 10.28±2.80% and 10.98±1.99%, respectively) and caspase-3 activity in the myocardium (0.62±0.02 OD/mg to 0.38±0.02 OD/mg and 0.32±0.02 OD/mg, respectively), showing their protective effects upon cardiomyocytes; and (v) DSD and STA had similar protective effects on I/R injury as those seen with the positive control metoprolol. In vitro, DSD and STA could significantly decrease the apoptosis of neonatal cardiomyocytes.<h4>Conclusions/significance</h4>These data suggest that DSD and STA can protect against myocardial I/R injury. The underlining mechanism may be related to their role in inhibiting cardiomyocyte apoptosis.Ruimiao ChangYong LiXingxin YangYuan YueLili DouYanwei WangWeifang ZhangXiaoni LiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 4, p e61590 (2013) |
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Medicine R Science Q Ruimiao Chang Yong Li Xingxin Yang Yuan Yue Lili Dou Yanwei Wang Weifang Zhang Xiaoni Li Protective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats. |
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<h4>Background</h4>Our previous studies suggested that deoxyschizandrin (DSD) and schisantherin A (STA) may have cardioprotective effects, but information in this regard is lacking. Therefore, we explored the protective role of DSD and STA in myocardial ischemia-reperfusion (I/R) injury.<h4>Methodology/principal findings</h4>Anesthetized male rats were treated once with DSD and STA (each 40 µmol/kg) through the tail vein after 45 min of ischemia, followed by 2-h reperfusion. Cardiac function, infarct size, biochemical markers, histopathology and apoptosis were measured and mRNA expression of gp91 (phox) in myocardial tissue assessed by RT-PCR. Neonatal rat cardiomyocytes were pretreated with DSD and STA and then damaged by H2O2. Cell apoptosis was tested by a flow cytometric assay. Compared with the I/R group: (i) DSD and STA could significantly reduce the abnormalities of LVSP, LVEDP, ±dp/dtmax and arrhythmias, thereby showing their protective roles in cardiac function; (ii) DSD and STA could significantly attenuate the infarct size and MDA release while increasing SOD activity, suggesting a role in reducing myocardial injury; (iii) tissue morphology and myocardial textual analysis revealed that DSD and STA mitigated changes in myocardial histopathology; (iv) DSD and STA decreased apoptosis (33.56±2.58% to 10.28±2.80% and 10.98±1.99%, respectively) and caspase-3 activity in the myocardium (0.62±0.02 OD/mg to 0.38±0.02 OD/mg and 0.32±0.02 OD/mg, respectively), showing their protective effects upon cardiomyocytes; and (v) DSD and STA had similar protective effects on I/R injury as those seen with the positive control metoprolol. In vitro, DSD and STA could significantly decrease the apoptosis of neonatal cardiomyocytes.<h4>Conclusions/significance</h4>These data suggest that DSD and STA can protect against myocardial I/R injury. The underlining mechanism may be related to their role in inhibiting cardiomyocyte apoptosis. |
format |
article |
author |
Ruimiao Chang Yong Li Xingxin Yang Yuan Yue Lili Dou Yanwei Wang Weifang Zhang Xiaoni Li |
author_facet |
Ruimiao Chang Yong Li Xingxin Yang Yuan Yue Lili Dou Yanwei Wang Weifang Zhang Xiaoni Li |
author_sort |
Ruimiao Chang |
title |
Protective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats. |
title_short |
Protective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats. |
title_full |
Protective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats. |
title_fullStr |
Protective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats. |
title_full_unstemmed |
Protective role of deoxyschizandrin and schisantherin A against myocardial ischemia-reperfusion injury in rats. |
title_sort |
protective role of deoxyschizandrin and schisantherin a against myocardial ischemia-reperfusion injury in rats. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2013 |
url |
https://doaj.org/article/f7934d4ad92a48119553113c5692b9a4 |
work_keys_str_mv |
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