Cardioprotective effects of bms-180448, a prototype mitokatp channel opener, and the role of salvage kinases, in the rat model of global ischemia and reperfusion heart injury

2007 ◽  
Vol 30 (5) ◽  
pp. 634-640 ◽  
Author(s):  
Ju-Han Lee ◽  
In-Sang Jung ◽  
Sung-Hun Lee ◽  
Min-Kyu Yang ◽  
Ji-Hye Hwang ◽  
...  
Keyword(s):  
Rat Model ◽  
Global Ischemia ◽  
Ischemia And Reperfusion ◽  
Channel Opener ◽  
Mitokatp Channel ◽  
Cardioprotective Effects ◽  
Heart Injury

Cardioprotective Effects of [5-(2-Methyl-5-Fluorophenyl)furan-2-ylcarbonyl]guanidine (KR-32568) in an Anesthetized Rat Model of Ischemia and Reperfusion Heart Injury

Pharmacology ◽  
2005 ◽  
Vol 75 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Hui-Yul Roh ◽  
In-Sang Jung ◽  
Jung-Woo Park ◽  
Yeo-Pyo Yun ◽  
Kyu-Yang Yi ◽  
...  
Keyword(s):  
Rat Model ◽  
Ischemia And Reperfusion ◽  
Cardioprotective Effects ◽  
Heart Injury

Differential cardioprotective effects of cardiac and non-cardiac adenosine during global ischemia and reperfusion

2007 ◽  
Vol 42 (6) ◽  
pp. S201-S202
Author(s):  
Anwar S. Abd-Elfattah ◽  
Mai Ding ◽  
S. Jamal Mustafa ◽  
Magda A. Mansour ◽  
Farid R. Nomair
Keyword(s):  
Global Ischemia ◽  
Ischemia And Reperfusion ◽  
Cardioprotective Effects

scholarly journals Cardioprotective Effects of 20(S)-Ginsenoside Rh2 against Doxorubicin-Induced CardiotoxicityIn VitroandIn Vivo

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Hongbo Wang ◽  
Pengfei Yu ◽  
Haitao Gou ◽  
Jianqiao Zhang ◽  
Mei Zhu ◽  
...  
Keyword(s):  
Rat Model ◽  
A549 Cells ◽  
H9c2 Cell ◽  
Protective Agent ◽  
Protective Effects ◽  
Ginsenoside Rh2 ◽  
Cardioprotective Effects ◽  
Heart Injury

Doxorubicin (DOX) is considered as one of the best antineoplastic agents. However, its clinical use is restricted by its associated cardiotoxicity, which is mediated by the production of reactive oxygen species. In this study, 20(S)-ginsenoside Rh2 (Rh2) was explored whether it had protective effects against DOX-induced cardiotoxicity.In vitrostudy on H9C2 cell line, as well asin vivoinvestigation in one mouse and one rat model of DOX-induced cardiomyopathy, was carried out. The results showed that pretreatment with Rh2 significantly increased the viability of DOX-injured H9C2 cells. In the mouse model, Rh2 could suppress the DOX-induced release of the cardiac enzymes into serum and improved the occurred pathological changes through ameliorating the decreased antioxidant biomolecules and the cumulated lipid peroxidation malondialdehyde in heart tissues. In the rat model, Rh2 could attenuate the change of ECG resulting from DOX administration. Furthermore, Rh2 enhanced the antitumor activity of DOX in A549 cells. Our findings thus demonstrated that Rh2 pretreatment could effectively alleviate heart injury induced by DOX, and Rh2 might act as a novel protective agent in the clinical usefulness of DOX.

scholarly journals Cardioprotective Effects of Osteopontin-1 during Development of Murine Ischemic Cardiomyopathy

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Georg D. Duerr ◽  
Bettina Mesenholl ◽  
Jan C. Heinemann ◽  
Martin Zoerlein ◽  
Peter Huebener ◽  
...  
Keyword(s):  
Ischemic Cardiomyopathy ◽  
Ventricular Dysfunction ◽  
Cardiac Fibroblasts ◽  
Hibernating Myocardium ◽  
Matricellular Protein ◽  
Ischemia And Reperfusion ◽  
Myocardial Contractile ◽  
Cardioprotective Effects ◽  
Lower Expression

Repetitive brief ischemia and reperfusion (I/R) is associated with ventricular dysfunction in pathogenesis of murine ischemic cardiomyopathy and human hibernating myocardium. We investigated the role of matricellular protein osteopontin-1 (OPN) in murine model of repetitive I/R. One 15-min LAD-occlusion followed by reperfusion was performed daily over 3, 5, and 7 consecutive days in C57/Bl6 wildtype- (WT-) and OPN−/−-mice (n=8/group). After echocardiography hearts were processed for histological and mRNA-studies. Cardiac fibroblasts were isolated, cultured, and stimulated with TGF-β1. WT-mice showed an early, strong, and cardiomyocyte-specific osteopontin-expression leading to interstitial macrophage infiltration and consecutive fibrosis after 7 days I/R in absence of myocardial infarction. In contrast, OPN−/−-mice showed small, nontransmural infarctions after 3 days I/R associated with significantly worse ventricular dysfunction. OPN−/−-mice had different expression of myocardial contractile elements and antioxidative mediators and a lower expression of chemokines during I/R. OPN−/−-mice showed predominant collagen deposition in macrophage-rich small infarctions. We found lower induction of tenascin-C, MMP-9, MMP-12, and TIMP-1, whereas MMP-13-expression was higher in OPN−/−-mice. Cultured OPN−/−-myofibroblasts confirmed these findings. In conclusion, osteopontin seems to modulate expression of contractile elements, antioxidative mediators, and inflammatory response and subsequently remodel in order to protect cardiomyocytes in murine ischemic cardiomyopathy.

Sign in / Sign up

Export Citation Format

Share Document