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机构地区:[1]广西医科大学第一附属医院,南宁530021 [2]广西壮族自治区卫生厅,南宁530021
出 处:《基因组学与应用生物学》2014年第5期970-974,共5页Genomics and Applied Biology
基 金:国家自然科学基金(81060070);广西自然科学基金(2012GXNSFAA053083)共同资助
摘 要:姜黄素是从姜科植物姜黄的根茎中提取的多酚类物质,具有重要的药用价值。本研究将30只健康雄性Wistar大鼠,随机分为3组:正常对照组(n=10)、糖尿病模型组(n=10)、糖尿病模型+姜黄素治疗组(n=10简称姜黄素治疗组)。以LPS(300ug·kg·-1day·-1)皮下注射8周建立2型糖尿病模型。测定空腹血糖逸11.1 mmol/L诊断为糖尿病。造模成功后,予姜黄素200 mg/(kg·-1day·-1)灌胃。连续治疗8周后,观察各组动物的一般情况,进行口服糖耐量试验(OGTT)及采用16S rRNA基因扩增子测序比较各组大鼠的肠道菌群。研究姜黄素对脂多糖(lipopolysaccharide,LPS)诱导糖尿病大鼠肠道菌群的影响。结果表明:姜黄素可改善LPS所致糖尿病大鼠的多饮、多食等症状并对糖耐量有明显的改善(p<0.05)。LPS诱导的糖尿病大鼠肠道中提升的Melainabacteria含量可被姜黄素灌服降低(p<0.05)。本研究揭示姜黄素具有降低LPS诱导的糖尿病大鼠血糖的作用,其机制可能与调节肠道微生态有关。Curcumin is kind of Polyphenols or pigments extracted fi'om curcuma zingileraceae plants with great medicinal effects. In present study, thirty healthy male Wistar rats were randomly divided into three groups, a normal control group (n=10), a model group (n=10), and an curcumin treated group (n=10). The rat model of diabetic were made by LPS induced with (300 μg·kg·-1day·-1) subcutaneous injection in 8 weeks. The symptom of diabetes was di- agnosed while the fasting blood glucose (FBG) level reached 11.1 mmol/L or more, and then the groups were treated with curcumin 200 mg/(kg·-lday·-1) by gavage. After the treatment in eight weeks later, we observed and recorded the general status and symptom of the Wistar rats, and performed the oral glucose tolerance test (OGTT) as well. Rat gut microbiome profiles by using 16S rRNA amplicon sequencing were also carried out in this research in order to assess the effect ofcurcumin on the gut microbiome of the Wistar rats with LPS induced type 2 diabets. The results showed that the curcumin could improve the endurance of the blood sugar in the rat models with diabetes caused by lipopolysaccharide (p〈0.05). The abundance of Melainabacteria in the gut of insulin resistance rats could be decreased by curcumin oral administration (p〈0.05). This study might reveal that the curcumin could improve glucose tolerance in lipopolysaccharide induced diabetic rats, cal imbalance. which proposed to modulate intestinal microecologi-
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