Nutrition (Burbank, Los Angeles County, Calif.) · 2020
Pterostilbene attenuates liver injury and oxidative stress in intrauterine growth-retarded weanling piglets.
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Zhang Hao, Chen Yanan, Chen Yueping, Ji Shuli, Jia Peilu, Xu Jianxiong, Li Yue, Wang Tian
Аннотация
OBJECTIVES: The aim of the present study was to investigate the potential of pterostilbene, a beneficial component primarily found in blueberries, to alleviate the intrauterine growth retardation (IUGR)-induced early liver injury and oxidative stress in a porcine model.
METHODS: Thirty-six IUGR piglets and an equal number of normal birth weight (NBW) counterparts received a diet with or without pterostilbene (250 mg/kg diet) during the first week post-weaning. Parameters related to the hepatic injury, oxidative stress, and antioxidant defense mechanisms were analyzed.
RESULTS: Relative to NBW, IUGR induced liver injury, which corresponded to increments in circulating alanine transaminase activity and hepatic apoptotic cell rate, superoxide radical generation, and the accumulation of oxidative damage products (P < 0.05). Administering pterostilbene reduced plasma transaminase activities, decreased hepatocyte apoptosis rate, and prevented the augmented levels of hepatic superoxide anion, 8-hydroxy-2 deoxyguanosine, and 4-hydroxynonenal-modified protein (P < 0.05). In terms of the hepatic antioxidant function, pterostilbene was efficient in improving the superoxide dismutase activity and the metabolic cycle between reduced glutathione and its oxidized form (P < 0.05). The pterostilbene-supplemented diet facilitated the nuclear translocation of nuclear factor erythroid-2-related factor 2 (NRF2) and promoted the expression levels of superoxide dismutase 2 in the liver of IUGR piglets (P < 0.05).
CONCLUSION: This study indicates that pterostilbene treatment has an auxiliary therapeutic potential to ameliorate early liver injury in IUGR neonates, presumably by stimulating the NRF2 signals and the associated antioxidant function.
METHODS: Thirty-six IUGR piglets and an equal number of normal birth weight (NBW) counterparts received a diet with or without pterostilbene (250 mg/kg diet) during the first week post-weaning. Parameters related to the hepatic injury, oxidative stress, and antioxidant defense mechanisms were analyzed.
RESULTS: Relative to NBW, IUGR induced liver injury, which corresponded to increments in circulating alanine transaminase activity and hepatic apoptotic cell rate, superoxide radical generation, and the accumulation of oxidative damage products (P < 0.05). Administering pterostilbene reduced plasma transaminase activities, decreased hepatocyte apoptosis rate, and prevented the augmented levels of hepatic superoxide anion, 8-hydroxy-2 deoxyguanosine, and 4-hydroxynonenal-modified protein (P < 0.05). In terms of the hepatic antioxidant function, pterostilbene was efficient in improving the superoxide dismutase activity and the metabolic cycle between reduced glutathione and its oxidized form (P < 0.05). The pterostilbene-supplemented diet facilitated the nuclear translocation of nuclear factor erythroid-2-related factor 2 (NRF2) and promoted the expression levels of superoxide dismutase 2 in the liver of IUGR piglets (P < 0.05).
CONCLUSION: This study indicates that pterostilbene treatment has an auxiliary therapeutic potential to ameliorate early liver injury in IUGR neonates, presumably by stimulating the NRF2 signals and the associated antioxidant function.