In this report, we investigated the protective function of co-enzyme Q10 on chicken hearts during in vivo heat stress (HS) and the relationship with Hsp70 expression. The concentration of co-enzyme Q10 (Q10) in the serum indicated that Q10 exogenously added prior HS was fully absorbed by chickens and is maintained at high levels during HS. The level of heart and oxidative damage-associated enzymes in the serum revealed that treatment with Q10 decreased the activity of CK-MB, CK, and LDH compared with the HS group; moreover, oxidative injury was also alleviated by Q10 according to the level of SOD, MDA, and T-AOC in the serum compared with HS group during heat stress. A pathological examination indicated that the chicken hearts suffered serious damage during HS, including hemorrhage, granular changes, karyopyknosis, and cardiac muscle fiber disorder; however, the extent of heart damage was reduced in HS + Q10 group. Our results indicated that the addition of Q10 could upregulate the expression of Hsp70 during HS compared with the HS group. Compared with the HS group, the addition of Q10 significantly increased the gene expression of hsf1 during HS and hsf3 at 5 h of HS. The expression of hsf2 and hsf4 was not influenced by HS. Q10 could only accelerate the trimerization of HSF1 as well binding activities to Hsp70 HSE according to native page and ChIP assays. These findings suggest that co-enzyme Q10 can protect chicken hearts from in vivo HS by inducing HSF1 binding activity and Hsp70 expression.
Keywords: HSF1; Hsp70; chicken heart; co-enzyme Q10; heat stress.
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