| 1 | 高果糖、高脂喂养致小鼠肝脏内质网应激的时程变化显示文摘目的探讨高果糖与高脂饮食对比诱导的小鼠肝脏内质网应激(ERS)的发生时程变化。方法雄性C57BL/J6小鼠分为对照组、高果糖组及高脂组,分别在喂养3 d、8 w后测定各组小鼠空腹血糖(FPG)、空腹血清胰岛素(FINS)、肝脏甘油三酯(TG)含量,并测定各组小鼠肝脏ERS标志物——磷酸化胰腺内质网激酶(p-PERK)及磷酸化山梨醇要求激酶-1(p-IRE1/t-IRE1)的蛋白表达。结果喂养3 d后,与对照组相比,两组FPG、FINS无明显变化,而肝TG水平均显著增加;喂养8 w后,与对照组相比,两组FPG、FINS、肝TG水平均显著增加;喂养3 d后,与对照组相比,高果糖组的肝内p-PERK、p-IRE1蛋白表达显著增加,提示出现ERS,而高脂组GRP78、p-PERK的蛋白表达与对照组无显著区别;喂养8 w后,高果糖、高脂组的肝内p-PERK、p-IRE1蛋白表达均显著增加。结论短期和长期高果糖和高脂喂养均可引起肝内脂质沉积,但高果糖喂养小鼠在脂肪肝发生早期即可出现肝ERS,而高脂喂养小鼠则在长期喂养后方出现肝ERS,提示ERS与高果糖、高脂饮食诱导的脂肪肝发生发展均有关,但介导机制不同。 | 任路平 于贤 宋光耀 孙文 李凡 陈树春 | 2015 | 中国老年学杂志2015，35，23： | 6 |
| 2 | Resveratrol and fenofibrate ameliorate fructose-induced nonalcoholic steatohepatitis by modulation of genes expression显示文摘AIM: To evaluate the effect of resveratrol, alone and in combination with fenofibrate, on fructose-induced metabolic genes abnormalities in rats. METHODS: Giving a fructose-enriched diet(FED) to rats for 12 wk was used as a model for inducing hepatic dyslipidemia and insulin resistance. Adult male albino rats(150-200 g) were divided into a control group and a FED group which was subdivided into 4 groups, a control FED, fenofibrate(FENO)(100 mg/kg), resveratrol(RES)(70 mg/kg) and combined treatment( FENO + RES)( half the doses). A l l treatments were given orally from the 9th week till the end of experimental period. Body weight, oral glucose tolerance test(OGTT), liver index, glucose, insulin, insulin resistance(HOMA), serum and liver triglycerides(TGs), oxidative stress(liver MDA, GSH and SOD),serum AST, ALT, AST/ALT ratio and tumor necrosis factor-α(TNF-α) were measured. Additionally, hepatic gene expression of suppressor of cytokine signaling-3(SOCS-3), sterol regulatory element binding protein-1c(SREBP-1c), fatty acid synthase(FAS), malonyl Co A decarboxylase(MCD), transforming growth factor-β1(TGF-β1) and adipose tissue genes expression of leptin and adiponectin were investigated. Liver sections were taken for histopathological examination and steatosis area were determined.RESULTS: Rats fed FED showed damaged liver, impairment of glucose tolerance, insulin resistance, ox ida t ive s t re s s a nd dy s l ipide m ia. As fo r ge ne expression, there was a change in favor of dyslipidemia and nonalcoholic steatohepatitis(NASH) development. All treatment regimens showed some benefit in reversing the described deviations. Fructose caused deterioration in hepatic gene expression of SOCS-3, SREBP-1c, FAS, MDA and TGF-β1 and in adipose tissue gene expression of leptin and adiponectin. Fructose showed also an increase in body weight, insulin resistance(OGTT, HOMA), serum and liver TGs, hepatic MDA, serum AST, AST/ALT ratio and TNF-α compared to control. All treatments improved SOCS-3, FAS, MCD, TGF-β1 and leptin genes expression while only RES and FENO + RES groups showed an improvement in SREBP-1c expression. Adiponectin gene expression was improved only by RES. A decrease in body weight, HOMA, liver TGs, AST/ALT ratio and TNF-α were observed in all treatment groups. Liver index was increased in FENO and FENO + RES groups. Serum TGs was improved only by FENO treatment. Liver MDA was improved by RES and FENO + RES treatments. FENO + RES group showed an increase in liver GSH content.CONCLUSION: When resveratrol was given with half the dose of fenofibrate it improved NASH-related fructose-induced disturbances in gene expression similar to a full dose of fenofibrate. | Enas A Abd El-Haleim Ashraf K Bahgat Samira Saleh | 2016 | World Journal of Gastroenterology2016，22，10： | 5 |
您所在的机构暂未开通此部分的功能，请联系管理员