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首页> 外文期刊>Nigerian Journal of Physiological Sciences >Effects of Maternal Dexamethasone Exposure During Lactation on Metabolic Imbalance and Oxidative Stress in the Liver of Male Offsprings of Wistar Rats
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Effects of Maternal Dexamethasone Exposure During Lactation on Metabolic Imbalance and Oxidative Stress in the Liver of Male Offsprings of Wistar Rats

机译：母体哺乳期地塞米松暴露对Wistar大鼠雄性子代肝脏代谢失衡和氧化应激的影响

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It has been reported in human and animal studies that early exposure to glucocorticoids could retard growth and subsequent development of cardio metabolic diseases. Chronic exposure to glucocorticoids induced oxidative stress. Therefore, the role of oxidative stress in some of the observed metabolic imbalance needs to be elucidated. This study examined the effects of lactational dexamethasone exposure on metabolic imbalance and oxidative stress marker in the liver of male offspring of exposed mother. Twenty lactating dams were divided into 4 groups of 5 animals each. Group 1 was administered 0.02 ml/100gbwt/day normal saline through lactation days 1-21. Group 2, 3, and 4 were administered 100 μg/kgbwt/day dexamethasone for lactation days 1-7, 1-14, and 1-21 respectively. The male offspring were thereafter separated and sacrificed at 12weeks of age for evaluation of lipid profile and oxidative stress marker in the liver. Results from this study indicate that Total Cholesterol (TC), Triglycerides (TAG) and LDL- cholesterol (LDL-C) were significantly (p<0.001) higher in the Dex 1-7, Dex 1-14 and Dex 1-21 groups when compared with the control. HDL-Cholesterol (HDL-C) was significantly (p<0.001) reduced in the Dex 1-7, Dex 1-14 and Dex 1-21 groups relative to the control. Basal Fasting Blood Sugar (FBS) was also significantly (p<0.001) higher in the Dex 1-14 and Dex 1-21 groups when compared with the control. Liver malondialdehyde was significantly (p<0.001) higher in the Dex1-14 and Dex1-21 group compared to the control. However, liver catalase and SOD activity were all significantly (p<0.001) lower in Dex 1-7, Dex 1-14 and Dex 1-21 groups relative to control. Liver protein was significantly (p<0.001) lower in the Dex1-14 and Dex1-21 treatment groups when compared with the control. Findings from this study suggest that there is possible increase in metabolic imbalance in the offspring of mother exposed to dexamethasone during lactation and these effects may be secondary to increase oxidative stress in the liver.
机译：在人和动物研究中已经报道过，早期暴露于糖皮质激素可能会延缓心脏代谢疾病的生长和随后的发展。长期暴露于糖皮质激素会引起氧化应激。因此，需要阐明氧化应激在某些观察到的代谢失衡中的作用。这项研究检查了暴露的地塞米松对暴露母亲的后代男性肝脏代谢失衡和氧化应激标志物的影响。将二十个泌乳水坝分为4组，每组5只动物。在哺乳第1至21天，第1组服用0.02 ml / 100gbwt /天的生理盐水。第2、3和4组分别在哺乳第1-7、1-14和1-21天服用100μg/ kgbwt /天的地塞米松。此后分离雄性后代并在12周龄处死以评估肝脏中的脂质分布和氧化应激标志物。这项研究的结果表明，在Dex 1-7，Dex 1-14和Dex 1-21组中，总胆固醇（TC），甘油三酸酯（TAG）和LDL-胆固醇（LDL-C）显着（p <0.001）高与对照相比。与对照相比，Dex 1-7，Dex 1-14和Dex 1-21组的HDL-胆固醇（HDL-C）显着降低（p <0.001）。与对照组相比，Dex 1-14和Dex 1-21组的基础空腹血糖（FBS）也显着较高（p <0.001）。与对照组相比，Dex1-14和Dex1-21组的肝丙二醛水平显着提高（p <0.001）。但是，相对于对照，Dex 1-7，Dex 1-14和Dex 1-21组的肝脏过氧化氢酶和SOD活性均显着降低（p <0.001）。与对照组相比，Dex1-14和Dex1-21治疗组的肝蛋白显着降低（p <0.001）。这项研究的发现表明，哺乳期间暴露于地塞米松的母亲的后代代谢失衡可能会增加，而这些影响可能是肝脏氧化应激增加的继发因素。

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