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

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.

Sub-Toxic Human Amylin Fragment Concentrations Promote the Survival and Proliferation of SH-SY5Y Cells via the Release of VEGF and HspB5 from Endothelial RBE4 Cells

“…The enhanced expression and secretion of HspB5 have been observed in different cell types, including endothelial cells [ 45 ]. Therefore, results obtained in the present study using CM to reduce amylin toxicity might be explained by the presence of HspB5 in the CM ( Figure 3 ), and our data are in agreement with literature data showing how an increased production of HspBs, and specifically HspB5, prevents cell death [ 46 , 47 , 48 ]. In particular, part of the protective effects observed in SH-SY5Y cells may depend on the ability of HspB5 in counteracting the aggregation of amyloid peptides [ 49 , 50 ], and thus, the formation of more toxic species such as the oligomers [ 26 ].…”

Vitamin C mitigates heat damage by reducing oxidative stress, inducing HSP expression in TM4 Sertoli cells

“…Furthermore, the ability of HSPs to scavenge ROS and maintain a redox balance is well-recognized (Tian et al, 2016;Venkatakrishnan, Cardounel, Zweier, Kuppusamy, & Llangovan, 2006). Our previous studies have reported that pretreatment with aspirin or coenzyme Q10 can induce HSP expression, consequently enhancing the heat resistance of the heart tissue and cardiomyocytes (Tang et al, 2014;Tang et al, 2016;Xu, Tang, Song, Yin, & Wu, 2017).…”

Vitamin C and sodium bicarbonate enhance the antioxidant ability of H9C2 cells and induce HSPs to relieve heat stress

“…Heat stress is a major environmental issue exacerbated by global warming that influences human health, affects animal growth and development, decreasing livestock production and causing sudden death in extreme cases (Crandall and Wilson 2014;Niu et al 2009). Heat stress can also damage important organs like the heart (Cui and Sinoway 2014;Tang et al 2016b) and induce tissue damage associated with sudden death. Heat stress can also destroy the integrity of the tight junctions of myocardial cells, and injure the structure and function of cell membranes (Aitken-Buck and Lamberts 2017; Crandall and Wilson 2014;Cui and Sinoway 2014).…”