Asiedu Bernice, Lembede Busisani Wiseman, Nyakudya Trevor Tapiwa, Chivandi Eliton
School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Parktown, South Africa.
Department of Physiology, School of Medicine, Faculty of Health Sciences, University of Pretoria, Gezina, South Africa.
Drug Chem Toxicol. 2023 Nov;46(4):736-745. doi: 10.1080/01480545.2022.2085740. Epub 2022 Jun 23.
Neonatal alcohol exposure (NAE) can induce oxidative stress. We determined whether zingerone (ZO), a phytochemical with anti-oxidant activity, can mitigate the negative impact of neonatal alcohol-induced oxidative stress. Seventy ten-day-old Sprague-Dawley rat pups (35 male, 35 female) were randomly assigned and administered the following treatment regimens daily from postnatal day (PND) 12-21: group 1 - nutritive milk (NM), group 2 - NM +1 g/kg ethanol (Eth), group 3 - NM + 40 mg/kg ZO, group 4 - NM + Eth + ZO. Growth performance, blood glucose and plasma triglycerides (TGs), total cholesterol, HDL-cholesterol, leptin and insulin concentration were determined. Cytochrome p450E21(CYP2E1) and thiobarbituric acid (TBARS); markers of hepatic oxidative stress and catalase, superoxide dismutase (SOD) and total glutathione (GSH), anti-oxidant markers of the pups were determined. Oral administration of ethanol (NM + Eth), zingerone (NM + ZO) and combined ethanol and zingerone (NM + Eth + ZO) did not affect the growth performance and insulin and leptin concentration of the rats ( > 0.05). Ethanol significantly reduced plasma TGs concentration of female rats ( = 0.04 vs control). However, ethanol and/or its combination with zingerone decreased hepatic GSH ( = 0.02 vs control) and increased CYP2E1 ( = 0.0002 vs control) activity in male rat pups. Zingerone had no effect ( > 0.05 vs control) on the rats' CYP2E1, GSH, SOD and catalase activities. Neonatal alcohol administration elicited hepatic oxidative stress in male rat pups only, showing sexual dimorphism. Zingerone (NM + ZO) prevented an increase in CYP2E1 activity and a decrease in GSH concentration but did not prevent the alcohol-induced hepatic oxidative stress in the male rat pups.
新生儿酒精暴露（NAE）可诱导氧化应激。我们确定了姜辣素（ZO）这种具有抗氧化活性的植物化学物质是否能够减轻新生儿酒精诱导的氧化应激的负面影响。70只10日龄的斯普拉格-道利大鼠幼崽（35只雄性，35只雌性）被随机分配，并从出生后第12天至第21天每天给予以下治疗方案：第1组——营养奶（NM），第2组——NM + 1 g/kg乙醇（Eth），第3组——NM + 40 mg/kg ZO，第4组——NM + Eth + ZO。测定生长性能、血糖和血浆甘油三酯（TGs）、总胆固醇、高密度脂蛋白胆固醇、瘦素和胰岛素浓度。测定细胞色素p450E21（CYP2E1）和硫代巴比妥酸（TBARS）；肝脏氧化应激标志物以及过氧化氢酶、超氧化物歧化酶（SOD）和总谷胱甘肽（GSH），即幼崽的抗氧化标志物。口服乙醇（NM + Eth）、姜辣素（NM + ZO）以及乙醇和姜辣素联合使用（NM + Eth + ZO）对大鼠的生长性能、胰岛素和瘦素浓度没有影响（P＞0.05）。乙醇显著降低了雌性大鼠的血浆TGs浓度（P = 0.04 vs对照组）。然而，乙醇和/或其与姜辣素的联合使用降低了雄性大鼠幼崽肝脏中的GSH（P = 0.02 vs对照组）并增加了CYP2E1活性（P = 0.0002 vs对照组）。姜辣素对大鼠的CYP2E1、GSH、SOD和过氧化氢酶活性没有影响（P＞0.05 vs对照组）。新生儿酒精给药仅在雄性大鼠幼崽中引发肝脏氧化应激，表现出性别差异。姜辣素（NM + ZO）可防止CYP2E1活性增加和GSH浓度降低，但不能防止雄性大鼠幼崽中酒精诱导的肝脏氧化应激。
