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| 1 | Silybin counteracts lipid excess and oxidative stress in cultured steatotic hepatic cells显示文摘AIM: To investigate in vitro the therapeutic effect and mechanisms of silybin in a cellular model of hepatic steatosis.METHODS: Rat hepatoma Fa O cells were loaded with lipids by exposure to 0.75 mmol/L oleate/palmitate for 3 h to mimic liver steatosis. Then, the steatotic cells were incubated for 24 h with different concentrations(25 to 100 μmol/L) of silybin as phytosome complex with vitamin E. The effects of silybin on lipid accumulation and metabolism, and on indices of oxidative stress were evaluated by absorption and fluorescence microscopy, quantitative real-time PCR, Western blot, spectrophotometric and fluorimetric assays.RESULTS: Lipid-loading resulted in intracellular triglyceride(TG) accumulation inside lipid droplets, whose number and size increased. TG accumulation was mediated by increased levels of peroxisome proliferator-activated receptors(PPARs) and sterol regulatory element-binding protein-1c(SREBP-1c). The lipid imbalance was associated with higher production of reactive oxygen species(ROS) resulting in increased lipid peroxidation, stimulation of catalase activity and activation of nuclear factor kappa-B(NF-κB). Incubation of steatotic cells with silybin 50 μmol/L significantly reduced TG accumulation likely by promoting lipid catabolism and by inhibiting lipogenic pathways, as suggested by the changes in carnitine palmitoyltransferase 1(CPT-1), PPAR and SREBP-1c levels. The reduction in fat accumulation exerted by silybin in the steatotic cells was associated with the improvement of the oxidative imbalance caused by lipid excess as demonstrated by the reduction in ROS content, lipid peroxidation, catalase activity and NF-κB activation.CONCLUSION: We demonstrated the direct antisteatotic and anti-oxidant effects of silybin in steatotic cells, thus elucidating at a cellular level the encouraging results demonstrated in clinical and animal studies. | Giulia Vecchione Elena Grasselli Adriana Voci Francesca Baldini Ignazio Grattagliano David QH Wang Piero Portincasa Laura Vergani | 2016 | World Journal of Gastroenterology2016，22，26： | 13 |
| 2 | 初诊2型糖尿病合并代谢综合征患者颈围与胰岛素抵抗、超敏C反应蛋白的相关性显示文摘目的:探讨2型糖尿病(type 2 diabetes mellitus,T2DM)合并代谢综合征(metabolic syndrome,MS)患者颈围与胰岛素抵抗、血清超敏C反应蛋白(hs-CRP)的关系。方法:选择研究对象165例,其中对照组55例,单纯2型糖尿病组(T2DM组)55例,T2DM合并MS组(MS组)55例。所有研究对象测量颈围,行口服葡萄糖耐量试验(OGTT)及胰岛素释放试验,并检测血脂、血清hs-CRP等相关生化指标。结果:MS组的颈围为(38.47±3.68)cm,大于正常对照组(35.17±3.09)cm及T2DM组(36.86±2.92)cm(P<0.05或P<0.01);MS组血清hs-CRP水平为[2.77(1.19~5.55)]mg/L,显著高于正常对照组[0.40(0.18~0.98)]mg/L及T2DM组[1.74(0.81~5.33)]mg/L(P<0.01)。随着颈围水平的升高,体质量指数(BMI)、腰围、腰臀比、空腹胰岛素(FINS)、餐后2h胰岛素(PSI)、三酰甘油、胰岛素抵抗指数(HOMA-IR)及hs-CRP水平显著升高,高密度脂蛋白胆固醇(HDL-C)水平显著降低。简单相关分析显示,颈围与BMI、腰围、腰臀比、舒张压、空腹血糖、餐后2h血糖(2hPG)、FINS、PSI、三酰甘油、低密度脂蛋白胆固醇(LDL-C)、HOMA-IR及hs-CRP呈正相关(P<0.05或P<0.01),与HDL-C呈显著负相关(P<0.01);Logistic回归分析显示,颈围、腰围、三酰甘油是T2DM合并MS的危险因素,HDL-C是其保护因素(P<0.01)。结论:新诊断T2DM合并MS患者颈围明显增加,其与胰岛素抵抗、血清hs-CRP水平密切相关,颈围是T2DM合并MS的危险因素。 | 钱唯韵 俞淑琴 朱天一 汤冰倩 孙文君 胡浩 叶菁菁 王东 王济芳 杨玲 袁国跃 | 2014 | 江苏大学学报(医学版)2014，24，3： | 6 |
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