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首页> 外文期刊>European review for medical and pharmacological sciences. >The influence of palatable high-energy diet in diet-induced obesity pregnant rats on offspring oxidative stress in liver
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The influence of palatable high-energy diet in diet-induced obesity pregnant rats on offspring oxidative stress in liver

机译:饮食诱发的肥胖妊娠大鼠可口的高能饮食对肝脏后代氧化应激的影响

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OBJECTIVE: We established an animal model of diet-induced obesity pregnant rats and their offsprings, and explored the effect of high-energy feeding on oxidative stress in filial rat liver, as well as the underlying mechanism. MATERIALS AND METHODS: Pregnant female Sprague-Dawley (SD) rats were randomly assigned into two groups: control group and palatable high-energy diet (PHED) group. Liver tissues were obtained 12 days after offspring rats were born for further study. The expressions of malondialdehyde (MDA), reduced glutathione (GSH) and antioxidative enzyme activities were measured, and pathological change of liver tissues was examined by HE staining. In addition, the expressions of inflammatory factors, tumor necrosis factor-α (TNF-α), IL-1β, and mRNA level of Heme oxygenase-1 (HO-1), were examined by ELISA and RT-PCR, respectively. Furthermore, COX-2 and nuclear factor kappa B (NF-κB) expressions were also examined by Western Blot. RESULTS: Offspring rats of PHED group displayed a significantly higher level of MDA than the control group, and significantly lower level of GSH. Significant reductions in the activities of a number of antioxidant enzymes, such as glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), were found in the PHED group offspring rats compared to the control group offspring rats. HE staining showed the liver cells in the control group offspring rats showed normal histopathological appearance, such as well-aligned cell patterning and unchanged cellular structure, but in the PHED group offspring rats showed slight structure deformation and misalignment. HO-1 mRNA in PHED group offspring rats is significantly higher than that in the control group offspring rats. Also, the expression of COX-2 and p-NF-κB-p65 in PHED group offspring rat liver is 72% and 38% higher than in the control group offspring rat liver, respectively. Expression of NF-κB-p65 in PHED group offspring rats is also significantly higher than that in the control group offspring rats. CONCLUSIONS: Palatable high-energy intake of obesity pregnant rats could lead to reduced antioxidant function in offspring rat liver, even increase the chance of chronical liver disease in the early ages of offsprings. The underlying mechanism is associated with the activity of NF-κB protein.
机译:目的:建立饮食诱导型肥胖妊娠大鼠及其后代的动物模型,探讨高能喂养对子代大鼠肝脏氧化应激的影响及其潜在机制。材料与方法:将雌性Sprague-Dawley(SD)雌性大鼠随机分为两组:对照组和可口的高能饮食(PHED)组。在后代大鼠出生后12天获得肝组织,以供进一步研究。检测丙二醛(MDA),还原型谷胱甘肽(GSH)和抗氧化酶的表达,并通过HE染色检查肝脏组织的病理变化。此外,分别通过ELISA和RT-PCR检测炎症因子,肿瘤坏死因子-α(TNF-α),IL-1β和血红素加氧酶-1(HO-1)的mRNA表达。此外,还通过蛋白质印迹检查了COX-2和核因子κB(NF-κB)的表达。结果:PHED组的后代大鼠MDA水平明显高于对照组,GSH水平明显低于对照组。在PHED组的后代大鼠中发现许多抗氧化剂酶的活性显着降低,例如谷胱甘肽S-转移酶(GST),超氧化物歧化酶(SOD),过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)。与对照组的后代大鼠相比。 HE染色显示,对照组后代大鼠的肝细胞显示出正常的组织病理学外观,例如排列良好的细胞图案和不变的细胞结构,但是在PHED组中后代大鼠显示出轻微的结构变形和错位。 PHED组后代大鼠的HO-1 mRNA显着高于对照组后代大鼠。而且,PHED组后代大鼠肝脏中COX-2和p-NF-κB-p65的表达分别比对照组后代大鼠肝脏高72%和38%。 PHED组后代大鼠中NF-κB-p65的表达也明显高于对照组。结论:肥胖妊娠大鼠高能量摄入可导致后代大鼠肝脏抗氧化功能降低,甚至增加后代早期患慢性肝病的机会。潜在的机制与NF-κB蛋白的活性有关。

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