scholarly journals Protective effect of glycyrrhizin on coronary microembolization‐induced myocardial dysfunction in rats

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Yonggang Yuan ◽  
Bing Li ◽  
Wanzhong Peng ◽  
Zesheng Xu
Keyword(s):  
Protective Effect ◽  
Myocardial Dysfunction ◽  
Coronary Microembolization

Myocardial dysfunction with coronary microembolization: Signal transduction through a sequence of no, TNFα and sphingosine

2002 ◽  
Vol 34 (6) ◽  
pp. A63
Author(s):  
Matthias Thielmann ◽  
Sergej Belosjorow ◽  
Claus Martin ◽  
Uwe Schwanke ◽  
Anita van de Sand ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Myocardial Dysfunction ◽  
Coronary Microembolization

Protective Effect of 3-Deazaadenosine in a Rat Model of Lipopolysaccharide-Induced Myocardial Dysfunction

Shock ◽  
2003 ◽  
Vol 19 (3) ◽  
pp. 245-251 ◽  
Author(s):  
Ruediger C. Braun-Dullaeus ◽  
Simon Dietrich ◽  
Michael J. Schoaff ◽  
Daniel G. Sedding ◽  
Boris Leithaeuser ◽  
...  
Keyword(s):  
Protective Effect ◽  
Rat Model ◽  
Myocardial Dysfunction

Resveratrol Attenuates Cardiomyocyte Apoptosis in Rats Induced by Coronary Microembolization Through SIRT1-Mediated Deacetylation of p53

2019 ◽  
Vol 24 (6) ◽  
pp. 551-558 ◽  
Author(s):  
Qing Mao ◽  
Xiulin Liang ◽  
Yufu Wu ◽  
Yongxiang Lu
Keyword(s):  
Cardiac Function ◽  
Caspase 3 ◽  
Troponin I ◽  
Myocardial Dysfunction ◽  
Picric Acid ◽  
Protective Role ◽  
Apoptotic Index ◽  
Cardiomyocyte Apoptosis ◽  
Sirtuin 1 ◽  
Coronary Microembolization

Objective: Coronary microembolization (CME)-induced cardiomyocyte apoptosis is the primary factor in causing cardiac dysfunction. Resveratrol (RES) is known to play a protective role in a variety of cardiovascular diseases, yet it is not known whether RES has a protective role in CME. Therefore, the effect of RES on cardiomyocyte apoptosis and cardiac function damage which are induced by CME in rats was investigated in this study. Methods: Fifty Sprague-Dawley rats were separated into 5 groups randomly (10 rats were included in each): sham group, CME group, RES+CME group, RES+CME+Sirtuin-1 (SIRT-1) inhibitor EX527 (RES+CME+EX) group, and CME+EX group. Cardiac function, serum c-troponin I (cTnI) level, apoptotic index, and microinfarct were measured by cardiac ultrasound, myocardial enzyme assessment, TdT-mediated dUTP Nick-end labeling and hematoxylin-basic fuchsin-picric acid staining. The levels of p53, p53 acetylation, SIRT-1, Bax, Bcl-2, and cleaved caspase-3 were detected by Western blot. Results: Myocardial dysfunction, enhanced apoptotic index as well as cTnI were caused after the operation of CME. Coronary microembolization induced increased expression of p53 acetylation and cleaved caspase-3, while the SIRT-1 and Bcl-2/Bax ratio was reduced. The CME effect was reversed by RES while EX527 attenuated this protective effect. Conclusions: Resveratrol can improve cardiac function, in the sense that it attenuates CME-induced cardiomyocyte apoptosis, which is perhaps associated with its inhibition pro-apoptotic pathway of p53 which is transcription-independent.

scholarly journals Mast Cell Contributes to Cardiomyocyte Apoptosis after Coronary Microembolization

2006 ◽  
Vol 54 (5) ◽  
pp. 515-523 ◽  
Author(s):  
Qing-Yong Zhang ◽  
Jun-Bo Ge ◽  
Jun-Zhu Chen ◽  
Jian-Hua Zhu ◽  
Liang-Hui Zhang ◽  
...  
Keyword(s):  
Baseline Level ◽  
Volume Fraction ◽  
Myocardial Dysfunction ◽  
Cardiomyocyte Apoptosis ◽  
Collagen Formation ◽  
Coronary Microembolization ◽  
Flow Reserve ◽  
Tnf Α ◽  
Pathophysiological Role ◽  
Factor Α

Coronary microembolization (CME) is associated with progressive myocardial dysfunction despite restoration of coronary flow reserve (CFR). The potential pathophysiological role of mast cells (MCs) remains unclear. Therefore, we induced CME in 18 miniswines and determined whether MC accumulation occurs and their effects on local cytokine secretion [interleukin (IL)-6, IL-8, tumor necrosis factor-α (TNF-α)]; cardiomyocyte apoptosis; and collagen formation at day 1 (D1), day 7 (D7), and day 30 (D30) after CME. Four sham-operated animals without CME (controls) and six animals treated with a MC stabilization agent (tranilast) for 30 days after CME were also studied. CFR decreased at D1 but returned to baseline level at D7 and D30. Coronary sinus levels of IL-6, IL-8, and TNF-α increased significantly at D1 and D7 ( p<0.01 vs baseline). Levels of IL-6 and IL-8 at D30 returned to baseline level, but not those of TNF-α. The numbers of total and degranulating MCs, % apoptotic cardiomyocytes, and collagen volume fraction (CVF) over CME myocardium at D1, D7, and D30 were significantly higher than controls ( p<0.01). Treatment with tranilast significantly reduced the serum level of TNF-α, numbers of total and degranulating MCs, % apoptotic cardiomyocytes, and CVF at D30 (all p<0.05). There was a significant positive correlation between the numbers of MCs with % apoptotic cardiomyocytes ( r = 0.77, p<0.001) and CVF ( r = 0.75, p<0.001) over the CME myocardium. Despite restoration of CFR, cardiomyocyte apoptosis persisted after CME and was positively correlated with the number of MCs but was prevented with tranilast treatment. These findings suggest that MCs contribute to cardiomyocyte apoptosis after CME. (J Histochem Cytochem 54:515-523, 2006)

357: THE PROTECTIVE EFFECT OF RHGH ON POST-RESUSCITATION MYOCARDIAL DYSFUNCTION

2018 ◽  
Vol 46 (1) ◽  
pp. 161-161
Author(s):  
Min Yang ◽  
Tianfeng Hua ◽  
jun li ◽  
yangyang zou ◽  
limin chen ◽  
...  
Keyword(s):  
Protective Effect ◽  
Myocardial Dysfunction

scholarly journals Glucocorticoid Treatment Prevents Progressive Myocardial Dysfunction Resulting From Experimental Coronary Microembolization

Circulation ◽  
2004 ◽  
Vol 109 (19) ◽  
pp. 2337-2342 ◽  
Author(s):  
Andreas Skyschally ◽  
Michael Haude ◽  
Hilmar Dörge ◽  
Matthias Thielmann ◽  
Alexej Duschin ◽  
...  
Keyword(s):  
Myocardial Dysfunction ◽  
Glucocorticoid Treatment ◽  
Coronary Microembolization

scholarly journals Oxidative modification of tropomyosin and myocardial dysfunction following coronary microembolization

2006 ◽  
Vol 27 (7) ◽  
pp. 875-881 ◽  
Author(s):  
Marcella Canton ◽  
Andreas Skyschally ◽  
Roberta Menabò ◽  
Kerstin Boengler ◽  
Petra Gres ◽  
...  
Keyword(s):  
Myocardial Dysfunction ◽  
Oxidative Modification ◽  
Coronary Microembolization
Sign in / Sign up

Export Citation Format

Share Document