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The influence of palatable high-energy diet in diet-induced obesity pregnant rats on offspring oxidative stress in liver.
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.
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.
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