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| 1 | Silymarin Attenuates Hepatic and Pancreatic Redox Imbalance Independent of Glycemic Regulation in the Alloxan-induced Diabetic Rat Model显示文摘Objective To evaluate the efficiency of silymarin(SMN) in modulating metabolic parameters and redox status in rats with type 1 diabetes mellitus(T1 DM).Methods Diabetes was induced by intraperitoneal injection of alloxan. The diabetic rats were administered with SMN at doses of 50 and 100 mg/kg body weight/d for 30 consecutive days. The rats were divided into the following four groups: vehicle control, diabetic(alloxan-treated), DS50(alloxan +50 mg/kg body weight/d of SMN), and DS100(alloxan + 100 mg/kg body weight/d of SMN) groups. The bodyweight and food and water intake were evaluated. After 30 d, the animals were euthanized and the blood was collected for measuring the serum levels of glucose, triacylglycerol(TAG), urea, and creatinine. The liver and pancreas were collected for measuring the activities of superoxide dismutase(SOD) and catalase(CAT), and the levels of carbonylated protein(PC). The pancreas sample was also used for histological analysis.Results SMN reduced hepatic(P < 0.001) and pancreatic(P < 0.001) protein damage and creatinine levels(P = 0.0141) in addition to decreasing food(P < 0.001) and water intake(P < 0.001). However,treatment with SMN did not improve beta-cell function or decrease blood glucose levels in diabetic rats.Conclusion SMN improved polyphagia and polydipsia, renal function, and protected the liver and pancreas against protein damage without affecting hyperglycemia in diabetic animals. | Miranda Laise Mara Oliveira Agostini Livia da Cunha Lima Wanderson Geraldo de Camini Fernanda Caetano Costa Daniela Caldeira | 2020 | Biomedical and Environmental Sciences2020，33，9： | 1 |
| 2 | Twf1基因对心肌细胞凋亡及NF-κB信号通路的影响研究显示文摘目的探讨抑制Twf1基因表达对高糖诱导的心肌细胞增殖、凋亡及NF-κB信号的影响。方法高糖刺激H9c2细胞,将H9c2细胞分为对照组(5.5 mmol/L的葡萄糖处理细胞)、NC组(瞬时转染无干扰作用的si RNA后用5.5 mmol/L的葡萄糖刺激细胞)、高糖组(瞬时转染无干扰作用的siRNA后用25 mmol/L的葡萄糖刺激细胞)和Twf1-siRNA组(瞬时转染干扰Twf1表达的siRNA后用25 mmol/L的葡萄糖刺激细胞)。Western blotting检测蛋白表达,CCK8检测细胞活力,流式细胞仪检测细胞凋亡率及ROS含量。结果高糖可引起H9c2细胞Twf1表达升高,转染Twf1-siRNA后H9c2细胞Twf1的表达明显降低;高糖组细胞活力低于NC组,细胞凋亡率、ROS含量及p-IκBα、Bax和TNF-α的表达均高于NC组,差异均有统计学意义(P<0.05);Twf1-siRNA组的细胞活力高于高糖组,细胞凋亡率、ROS含量及p-IκBα、Bax和TNF-α的表达均低于高糖组,差异均有统计学意义(P<0.05)。结论抑制H9c2细胞Twf1基因表达可逆转高糖诱导的细胞活力降低及凋亡的增加,其机制可能与细胞内ROS含量降低及NF-κB信号下调有关。 | 慕莉蓉 俞红梅 许欣 刘颖 惠超杰 | 2018 | 中国循证心血管医学杂志2018，10，12： | 0 |
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