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

Abstract

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.

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

“…Previously, we conducted a preliminary assessment of the protective capacity of ASA and the association with HspB1 in an animal model (Wu et al 2015). In the extracorporal study, we demonstrated consistent results in cultured myocardial cells.…”

“…Other studies illustrated the protective function of ASA in the cardiovascular system (Deharo et al 2014;Mahaffey et al 2013) and immune system (Javeed et al 2011). Moreover, recent experiments in our laboratory demonstrated that ASA pretreatment would provide significant protective effects to chicken myocardial cells in vivo, for instance, the heat stress-induced increases of myocardial cell damage-related enzymes such as CK-MB and LDH were significantly supressed, and the pathological changes of myocardial cells such as acute degeneration were also reduced (Wu et al 2015). ASA used as a painkiller was initially considered to function via platelet interactions (Patrono et al 2005).…”

“…The Di Wu and Miao Zhang contributed equally to this work. myocardial cells of chickens in our recent studies showed such changes as swollen in size, acute granular or vacuolar degeneration, and karyopyknosis (Wu et al 2015). All these injuries are indicative of the harmful effects that heat stress would cause to the breeding industries.…”

Aspirin-induced heat stress resistance in chicken myocardial cells can be suppressed by BAPTA-AM in vitro

“…The damages caused by heat stress to breeding industries have been explained in our previous works, especially the considerable economic loss on poultry breeding (Wu et al 2015(Wu et al , 2016. Previous research also has revealed that acute HS leads to cardiac dysfunction and other forms of myocardial cell damage (Tang et al 2013), and these effects are responsible for sudden infant death in animals and even in humans after HS exposure (Gathiram et al 1987(Gathiram et al , 1988Rai and Ambwany 1980).…”

“…HS exposure increases the permeability of myocardial cells, causing a series of enzymes such as isoenzyme creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) to be released from the myocardial cells (Ma et al 2013;Xue et al 2015). These enzymes are categorized as myocardial cell damage-related enzymes and are widely used as markers of myocardial cell injury (Saravanan et al 2013;Tang et al 2013;Wu et al 2015). In addition to these enzymes, histopathological or cytopathological damages are also commonly observed in myocardial cells after HS; for example, the cells may be swollen in size, show uneven matrix staining in the cytoplasm, appear shrunken and dull-stained in the nucleus, or exhibit acute degeneration (Tang et al 2013;Wu et al 2015).…”