N-acetylcysteine Improves Cardiac Contractility and Ameliorates Myocardial Injury in a Rat Model of Lung Ischemia and Reperfusion Injury

Wu, Nan‐Chun; Chen, T.-H.; Yang, Y.-C.; Liao, F.-T.; Wang, J.-C.

doi:10.1016/j.transproceed.2013.09.005

Cited by 6 publications

(7 citation statements)

References 16 publications

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“…As reported, upon exposure to heat stress, the permeability of the myocardial cell membrane will increase and lead to extracellular release of a series of enzymes, including CK-MB and LDH. These enzymes are generally designated as cardiomyocyte damage-related enzymes and further regarded as important indicators for judging acute myocardial injury (Amani et al 2013;Chen et al 2013;Chon et al 2013;Wu et al 2013), especially CK-MB (Zeren et al 2013). In addition to these enzymes, cytopathological changes like swollen in size, uneven staining in the cytoplasm and vacuolar degeneration were clearly identified in a lot of researches (Chen et al 2015;Tang et al 2013).…”

Section: Discussionmentioning

confidence: 99%

In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells

Zhang

et al. 2016

Cell Stress and Chaperones

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To understand the potential association of heat stress resistance with HspB1 induction by aspirin (ASA) in chicken myocardial cells, variations of HspB1 expression and heat stressed-induced damage of myocardial cells after ASA administration were studied in primary cultured myocardial cells. Cytopathological lesions as well as damage-related enzymes, such as creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), indicated the considerable protective ability of ASA pre-treatment against acute heat stress. Immunostaining assays showed that heat stress caused HspB1 to relocate into the nucleus, while ASA did not. ELISA analysis, revealed that HspB1 expression induced by ASA averaged 45.62-fold higher than that of the control. These results indicated that the acute heat-stressed injuries were accompanied by comparatively lower HspB1 expression caused by heat stress in vitro. ASA pretreatment induced a level of HspB1 presumed to be sufficient to protect myocardial cells from acute heat stress in the extracorporal model, although more detailed mechanisms will require further investigation.

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Section: Discussionmentioning

confidence: 99%

In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells

Zhang

et al. 2016

Cell Stress and Chaperones

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“…The membrane permeability of myocardial cells increases under heat stress and releases a series of enzymes into the serum. These cardiomyocyte damage-related enzymes, such as CK-MB and LDH, are widely regarded as indicators of acute myocardial injury (Amani et al 2013;Chen et al 2013;Chon et al 2013;Wu et al 2013), especially enzyme CK-MB (Zeren et al 2013). In the present study, we examined pathological lesions and cardiomyocyte damage-related enzyme concentrations to detect myocardial cell injury in chickens exposed to high temperatures.…”

Section: Discussionmentioning

confidence: 99%

“…During heat stress, the membrane permeability of myocardial cells increases and enzymes are released from myocardial cells into the serum (Mitchell and Sandercock 1995;Saravanan et al 2013;Tang et al 2013). These enzymes, including isoenzyme creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), are widely regarded as indicators of acute myocardial injury (Amani et al 2013;Chen et al 2013;Chon et al 2013;Wu et al 2013;Zeren et al 2013). When exposed to elevated temperatures, animal cells synthesize a small number of highly conserved proteins called heat-shock proteins (Hsps) (Lindquist 1986).…”

Section: Introductionmentioning

confidence: 99%

Acetyl salicylic acid protected against heat stress damage in chicken myocardial cells and may associate with induced Hsp27 expression

Song

et al. 2015

Cell Stress and Chaperones

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We investigated whether acetyl salicylic acid (ASA) protects chicken myocardial cells from heat stress-mediated damage in vivo and whether the induction of Hsp27 expression is connected with this function. Pathological changes, damage-related enzyme levels, and Hsp27 expression were studied in chickens following heat stress (40 ± 1 °C for 0, 1, 2, 3, 5, 7, 10, 15, or 24 h, respectively) with or without ASA administration (1 mg/kg BW, 2 h prior). Appearance of pathological lesions such as degenerations and karyopyknosis as well as the myocardial damage-related enzyme activation indicated that heat stress causes considerable injury to the myocardial cells in vivo. Myocardial cell injury was most serious in chickens exposed to heat stress without prior ASA administration; meanwhile, ASA pretreatment acted protective function against high temperature-induced injury. Hsp27 expression was induced under all experimental conditions but was one-fold higher in the ASA-pretreated animals (0.3138 ± 0.0340 ng/mL) than in untreated animals (0.1437 ± 0.0476 ng/mL) 1 h after heat stress exposure, and such an increase was sustained over the length of the experiment. Our findings indicate that pretreatment with ASA protects chicken myocardial cells from acute heat stress in vivo with almost no obvious side effects, and this protection may involve an enhancement of Hsp27 expression. However, the detailed mechanisms underlying this effect require further investigation.

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“…Study of Wu et al, demonstrated that the NAC administration reduced lung I/R-induced increases in myocardial hydroxyl radical production and lipid peroxidation and ameliorated LV contractility and stiffening [ 62 ].…”

Section: N-acetylcysteinementioning

confidence: 99%

Oxidative Stress and Lung Ischemia-Reperfusion Injury

Ferrari

Andrade

2015

Oxidative Medicine and Cellular Longevity

212

189

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Ischemia-reperfusion (IR) injury is directly related to the formation of reactive oxygen species (ROS), endothelial cell injury, increased vascular permeability, and the activation of neutrophils and platelets, cytokines, and the complement system. Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury. Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection. Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients.

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N-acetylcysteine Improves Cardiac Contractility and Ameliorates Myocardial Injury in a Rat Model of Lung Ischemia and Reperfusion Injury

Cited by 6 publications

References 16 publications

In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells

In vitro evaluation of aspirin-induced HspB1 against heat stress damage in chicken myocardial cells

Acetyl salicylic acid protected against heat stress damage in chicken myocardial cells and may associate with induced Hsp27 expression

Oxidative Stress and Lung Ischemia-Reperfusion Injury

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