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NO-1886对过氧化体增殖物激活型受体、脂蛋白脂肪酶和肿瘤坏死因子α基因表达的影响

Effects of NO-1886 on Expression of Peroxisome Proliferator-Activated Receptor, Lipoprotein Lipase and Tumor Necrosis Factor-α
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摘要 为了探讨脂蛋白脂肪酶活化剂NO 1886对高脂高糖饮食喂养贵州小香猪过氧化物体增殖物激活型受体、脂蛋白脂肪酶及肿瘤坏死因子α表达的影响 ,选择雄性贵州小香猪 15头 ,随机分为 3组。正常对照组喂普通饲料 ;高脂高糖组喂高脂高蔗糖饲料 ;治疗组喂高脂高蔗糖饲料 4个月后加 1%NO 1886治疗。 8个月后处死动物 ,采用Trizol提取组织总RNA ,逆转录聚合酶链反应检测过氧化体增殖物激活型受体、脂蛋白脂肪酶及肿瘤坏死因子αmRNA的表达。结果发现 ,正常对照组肌肉组织和肝脏过氧化体增殖物激活型受体α的表达较低。高脂高糖组肌肉组织和肝脏过氧化体增殖物激活型受体α的表达增强 ,NO 1886使高脂高糖喂养增强肌肉组织和肝脏过氧化体增殖物激活型受体α表达的作用减弱 ;在脂肪组织 ,治疗组脂蛋白脂肪酶的表达水平最高 ,分别比正常对照组和高脂高糖组高 2 7%和 2 0 % ;NO 1886抑制高脂高糖喂养小香猪脂肪组织肿瘤坏死因子α的表达。结果提示 ,NO 1886能促进小香猪脂肪组织脂蛋白脂肪酶的表达 ,显著抑制脂肪组织肿瘤坏死因子α基因表达 ,高调脂肪组织过氧化体增殖物激活型受体γ ,减弱肝脏和肌肉过氧化体增殖物激活型受体α的表达 ,是NO 1886有效降低血浆游离脂肪酸和肿瘤坏死因子α水平可能的机制。 Aim To investigate the role of lipoprotein lipase ( LPL) activator NO-1886 on the mRNA expression of peroxisome proliferator-activated receptors (PPAR), LPL and tumor necrosis factor-α (TNF-α) in Guizhou minipigs fed with high-fat and high-sucrose. Methods Guizhou minipigs were randomized in to three groups: control group, high-fat high-sucrose group, high-fat high-sucrose and NO-1886 treated group (1% NO-1886 supplemented into the diet after 4 months). Reverse transcription-polymerase chain reaction (RT-PCR) analysis of PPAR, LPL and TNF-α RNA is extracted from frozen tissues, and reverse transcription-polymerase chain reaction (RT-PCR) is performed. Results The high-fat and high-sucrose diet increased the levels of mRNA expression of PPAR α in liver and muscle and the levels of mRNA expression of TNF-α in fat while decreased the levels of mRNA expression of fat PPAR α. NO-1886 improves the glucose metabolism probably through stimulating PPAR α and LPL expression. NO-1886 reduced the mRNA expression of fat TNF-α, decreased the mRNA expression of PPAR α in muscle and liver. Conclusions NO-1886 may stimulate PPAR γ and LPL expression, reduce the mRNA expression of TNF-α and PPAR α, which would account for an important role of NO-1886 in preventing atherosclerosis and lowing the blood sugar.
出处 《中国动脉硬化杂志》 CAS CSCD 2004年第4期387-391,共5页 Chinese Journal of Arteriosclerosis
基金 日本大制药厂新药研究基金 ( 2 0 0 1 8 2 8) 湖南省教育厅课题 (JY 0 1C193 )资助
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