检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
机构地区:[1]中国药科大学天然药物活性组分与药效国家重点实验室,南京210009
出 处:《西北药学杂志》2013年第3期278-281,共4页Northwest Pharmaceutical Journal
基 金:江苏高校优势学科建设工程资助项目
摘 要:目的探讨橙皮苷(hesperidin)对胰岛素抵抗HepG2细胞体外糖代谢的影响。方法采用高浓度胰岛素(INS)持续作用HepG2 12h建立胰岛素抵抗(IR-HepG2)模型,同时培养液中给予不同质量浓度橙皮苷(10,40和60μg.mL-1)或盐酸二甲双胍(30μg.mL-1)干预。药物作用12h后,换含低浓度INS的培养液培养细胞12h,使细胞同步化。然后,测定各组细胞葡萄糖消耗量、细胞内肝糖原含量、己糖激酶(hexokinase,HK)和丙酮酸激酶(pyruvate kinase,PK)的活力。结果与正常组相比,模型组细胞葡萄糖消耗量、肝糖原含量及HK和PK酶活力显著下降(P<0.01);与模型组相比,40和60μg.mL-1的橙皮苷可极显著增加IR-HepG2细胞葡萄糖消耗量、肝糖原合成量及HK酶活力(P<0.01),显著增加PK酶活力(P<0.05)。结论橙皮苷可增加IR-HepG2细胞对葡萄糖的利用,增加肝糖原合成量,提高HK、PK活力,从而促进IR-HepG2细胞糖代谢,改善胰岛素抵抗能力。Objective To investigate the effect of hesperidin on glycometabolism in insulin-resistance HepG2 cells. Methods The insu- lin resistant models of HepG2 cells (IR-HepG2) were induced by high concentration of insulin for 12 h,meanwhile,different con- centration of hesperidin (10,40 and 60 μg · mL^-1 ) or metformin (30 μg · mL^-1)was added into the cultured medium. After 12 hours,synchronized cells were made with low concentration of INS culture liquid to culture cells for 12 hours. Then, the glucose consumption, the liver glycogen synthesis, hexokinase(HK) and pyruvake kinase(PK) activity of each group cells were measured. Results Compared with the normal group, the glucose consumption, the liver glycogen synthesis, hexokinase (HK) and pyruvake kinase {PK} activity of IR group decreased significantly (P〈0.01). Compared with the IR group, the concentration of 40 and 60 μg · mL^-1 of hesperidin can significantly increase the glucose consumption,the liver glycogen synthesis,hexokinase ( HK) activity of IR-HepG2 ceils I P〈0.01 } ,increase pyruvake kinase (PK) activity of IR-HepG2 cells ( P〈0.05 ). Conclusion Hesperidin can improve the glucose consumptions, increase glycogen synthesis, and enhance HK and PK vitality in insulin-resistant model of HepG2 cells. Hesperidin may regulate the glucose metabolism and improve the insulin-resistant HepG2 cells.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.15