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目的探讨树豆酮酸A对HepG2细胞糖代谢影响及机制。方法体外培养HepG2细胞,实验设10-3、10-4、10-5、10-6mol/L树豆酮酸A组,作用24 h,采用葡萄糖氧化酶-过氧化物酶法检测HepG2细胞葡萄糖消耗量,ELISA法检测糖代谢相关酶己糖激酶(HK)和丙酮酸脱氢酶(PDH)活性。结果 10~(-3)、10~(-4)、10~(-5)mol/L树豆酮酸A组HepG2细胞葡萄糖消耗量分别为(8.650±0.319)、(8.231±0.182)、(8.136±0.402)mmol/L,明显高于对照组[(6.521±0.056)mmol/L],差异有统计学意义(P<0.05);10~(-3)、10~(-4)mol/L树豆酮酸A组HepG2细胞内HK含量分别为(882.91±30.72)、(718.25±20.67)pg/m L,明显高于对照组[(616.65±17.24)pg/m L];10-3mol/L树豆酮酸A组HepG2细胞内PDH含量为(1 526.69±66.74)pg/m L,明显高于对照组[(1 204.73±55.72)pg/m L],差异有统计学意义(P<0.05)。结论树豆酮酸A在体外可促进HepG2细胞对葡萄糖的摄取,具有降糖活性,其作用机制可能与增强糖代谢相关酶己糖激酶和丙酮酸脱氢酶活性有关。
Aim To investigate the effect and mechanism of SAA on HepG2 cell glucose metabolism. Methods HepG2 cells were cultured in vitro. The mice were treated with 10-3, 10-4, 10-5, 10-6mol / L SA for 24 hours. Glucose oxidase-peroxidase Consumption, and enzyme-linked immunosorbent assay (ELISA) to detect the activities of glucose metabolism related enzymes hexokinase (HK) and pyruvate dehydrogenase (PDH). Results The glucose consumption of HepG2 cells in 10 ~ (-3), 10 ~ (-4) and 10 ~ (-5) mol / L groups was (8.650 ± 0.319), (8.231 ± 0.182) 8.136 ± 0.402) mmol / L, which was significantly higher than that of the control group [(6.521 ± 0.056) mmol / L] (P <0.05) The HK contents of HepG2 cells in the L group were (882.91 ± 30.72) and (718.25 ± 20.67) pg / m L, respectively, which were significantly higher than those in the control group [(616.65 ± 17.24) pg / m L] / L The level of PDH in HepG2 cells in group A was (526.69 ± 66.74) pg / m L, which was significantly higher than that in control group [(1 204.73 ± 55.72) pg / m L] (P <0.05). Conclusions SAA can promote the uptake of glucose by HepG2 cells in vitro, and has a hypoglycemic activity. The mechanism may be related to enhancing the activities of enzymes hexokinase and pyruvate dehydrogenase related to glucose metabolism.