Aspirin upregulates αB-Crystallin to protect the myocardium against heat stress in broiler chickens.

Shu Tang,Bin Yin,Erbao Song,Endong Bao,Joerg Hartung,Hongbo Chen,Yanfen Cheng,Xiaohui Zhang

doi:10.1038/srep37273

Abstract

We established in vivo and in vitro models to investigate the role of αB-Crystallin (CryAB) and assess the ability of aspirin (ASA) to protect the myocardium during prolonged heat stress. Thirty-day-old chickens were divided into three groups (n = 90): heat stress (HS, 40±1 °C); ASA(−)HS(+), 1 mg/kg ASA orally 2 h before heat stress; and ASA(+)HS(−), pretreated with aspirin, no heat stress (25 °C). Hearts were excised after 0, 1, 2, 3, 5, 7, 10, 15 and 24 h. Heat stress increased body temperature, though the ASA(−)HS(+) group had significantly higher temperatures than the ASA(+)HS(+) group at all time points. Compared to ASA(+)HS(+), the ASA(−)HS(+) group displayed increased sensitivity to heat stress. Pathological analysis revealed the ASA (+)HS(+) myocardium showed less severe changes (narrowed, chaotic fibers; fewer necrotic cells) than the ASA(−)HS(+) group (bleeding and extensive cell death). In vitro, ASA-pretreatment significantly increased primary chicken myocardial cell survival during heat stress. ELISAs indicated ASA induced CryAB in vivo to protect against heat stress-induced myocardial damage, but ASA did not induce CryAB in primary chicken myocardial cells. The mechanisms by which ASA induces the expression of CryAB in vivo and protects the myocardium during heat stress merit further research.

Highlights

We established in vivo and in vitro models to investigate the role of αB-Crystallin (CryAB) and assess the ability of aspirin (ASA) to protect the myocardium during prolonged heat stress
Both groups subjected to heat stress had higher rectal temperatures than the control group housed at RT (25 °C; Fig. 1); the ASA(−)HS(+) group had significantly higher body temperatures compared to the ASA(+)HS(+)group at all time points during heat stress (P < 0.05)
Pathological lesions, mainly due to necrosis, were observed in the rat myocardium after 40 min of heat stress in vivo, accompanied by lower CryAB expression, indicating CryAB may play an important role to protect the mammalian heart against heat stress[21]

Summary

Introduction

We established in vivo and in vitro models to investigate the role of αB-Crystallin (CryAB) and assess the ability of aspirin (ASA) to protect the myocardium during prolonged heat stress. According to our previous in vivo and in vitro research in rats, sudden death caused by heat stress (41 ± 1 °C) is primarily the result of pathological changes in the heart, such as necrosis and cell degeneration[9]. In relation to heat shock[13], but are known to be expressed during other stresses including exposure to cold[14], UV light[15], and during wound healing or tissue remodeling[16] Many members of this group perform chaperone function by stabilizing new proteins to ensure correct folding or by helping to refold proteins that were damaged by the cell stress[17]. The protective roles of Hsp[60] and other Hsps have not been fully investigated[24,25]

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