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Chronic oral administration of pine bark extract (flavangenol) attenuates brain and liver mRNA expressions of HSPs in heat-exposed chicks
Institution:1. Department of Agrobiological Science, Faculty of Agriculture, Ehime University, Matsuyama 790-8566, Japan;2. Department of Anatomy and Embryology, Ehime University Graduate School of Medicine, Toon, 791-0295 Ehime, Japan;3. Department of Animal and Poultry Sciences, Virginia Polytechnic Institute and State University, 24061, Blacksburg, Virginia, United States;1. Center of Excellence for Poultry Science, University of Arkansas, Fayetteville, AR 72701, USA;2. Faculty of Agriculture, Ibaraki University, Ibaraki 300-0393, Japan;1. Division for Arts and Science, Faculty of Arts and Science, Kyushu University, Fukuoka 819–0395, Japan;2. Laboratory of Regulation in Metabolism and Behavior, Faculty of Agriculture, Kyushu University, Fukuoka 812–8581, Japan;3. Institute for Veterinary, Animal and Biomedical Sciences, Massey University, Palmerston North, New Zealand
Abstract:Exposure to a high ambient temperature (HT) can cause heat stress, which has a huge negative impact on physiological functions. Cellular heat-shock response is activated upon exposure to HT for cellular maintenance and adaptation. In addition, antioxidants are used to support physiological functions under HT in a variety of organisms. Flavangenol, an extract of pine bark, is one of the most potent antioxidants with its complex mixture of polyphenols. In the current study, chronic (a single daily oral administration for 14 days) or acute (a single oral administration) oral administration of flavangenol was performed on chicks. Then the chicks were exposed to an acute HT (40±1 °C for 3 h) to examine the effect of flavangenol on the mRNA expression of heat-shock protein (HSP) in the brain and liver. Rectal temperature, plasma aspartate aminotransferase (AAT), a marker of liver damage, and plasma corticosterone as well as metabolites were also determined. HSP-70 and -90 mRNA expression, rectal temperature, plasma AAT and corticosterone were increased by HT. Interestingly, the chronic, but not the acute, administration of flavangenol caused a declining in the diencephalic mRNA expression of HSP-70 and -90 and plasma AAT in HT-exposed chicks. Moreover, the hepatic mRNA expression of HSP-90 was also significantly decreased by chronic oral administration of flavangenol in HT chicks. These results indicate that chronic, but not acute, oral administration of flavangenol attenuates HSP mRNA expression in the central and peripheral tissues due to its possible role in improving cellular protective functions during heat stress. The flavangenol-dependent decline in plasma AAT further suggests that liver damage induced by heat stress was minimized by flavangenol.
Keywords:Chicks  Heat stress  Flavangenol  Heat-shock protein gene
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