Abstract
To investigate the effect of pine bark extract (flavangenol) on rectal temperature, plasma corticosterone, metabolites and heat shock proteins (HSPs) mRNA expression in heat-exposed chicks. Heat-stress causes oxidative damage in different cells and tissues including the brain and has huge negative impact on cellular environment. However, cell possesses its own protective mechanisms to maintain the intracellular homeostasis. For example, heat-stress increases HSPs expression, which protects the cellular functions. Unfortunately, such an endogenous cellular protective mechanism may not be persisted under prolonged heat-stress. Thus, antioxidants are being used in the poultry industry to support the physiological functions of chickens under severe heat-stress. Flavangenol, an effective antioxidant, was used in our study to examine its anti-heat stress effects. Acute (single oral administration) or chronic (single oral administration/day for 14 days) administration of flavangenol was performed in chicks. Then the chicks were exposed to a high ambient temperature (HT; 40 ± 1°C for 3 h) or a control thermoneutral temperature (CT; 30 ± 1°C) to examine the effects of flavangenol on the mRNA expression of HSPs in the brain. Data were analyzed by factorial two-way analysis of variance (ANOVA) with respect to HT and treatment. We found that HT significantly increased HSP-70 and -90 mRNA expressions, rectal temperature, plasma corticosterone and aspartate aminotransferase (AAT) (P<0.05). Interestingly, it was further found that the chronic administration of flavangenol caused a dose-dependent declining in the diencephalic mRNA expression of HSP-70, HSP-90 and plasma AAT in heat-exposed chicks. These results indicate that chronic oral administration of flavangenol may attenuate HSPs mRNA expression in the central tissues due to its possible role in improving cellular protection during heat-stress. The flavangenol-dependent declining in plasma AAT in heat-exposed chicks further suggests that flavangenol played an important role to minimize heat-stress-induced damage.
Keywords: Heat shock protein, Antioxidant
