高级检索
张聪, 远航, 牛玉存. EGCG改善油酸诱导的SW872脂肪细胞胰岛素抵抗作用及机制[J]. 中国公共卫生, 2018, 34(1): 67-70. DOI: 10.11847/zgggws1115133
引用本文: 张聪, 远航, 牛玉存. EGCG改善油酸诱导的SW872脂肪细胞胰岛素抵抗作用及机制[J]. 中国公共卫生, 2018, 34(1): 67-70. DOI: 10.11847/zgggws1115133
Cong ZHANG, Hang YUAN, Yu-cun NIU. Effect and mechanism of EGCG on improving insulin resistance induced by oleic acid in SW872 adipocytes[J]. Chinese Journal of Public Health, 2018, 34(1): 67-70. DOI: 10.11847/zgggws1115133
Citation: Cong ZHANG, Hang YUAN, Yu-cun NIU. Effect and mechanism of EGCG on improving insulin resistance induced by oleic acid in SW872 adipocytes[J]. Chinese Journal of Public Health, 2018, 34(1): 67-70. DOI: 10.11847/zgggws1115133

EGCG改善油酸诱导的SW872脂肪细胞胰岛素抵抗作用及机制

Effect and mechanism of EGCG on improving insulin resistance induced by oleic acid in SW872 adipocytes

  • 摘要:
      目的  观察植物化学物表没食子儿茶素没食子酸酯(EGCG)对胰岛素抵抗SW872脂肪细胞葡萄糖转运、胰岛素敏感性及炎症因子表达作用。
      方法  利用油酸处理脂肪细胞诱导胰岛素抵抗模型,给予不同剂量EGCG(25、50、100 μmol/L)处理24 h,利用激光共聚焦显微镜检测2–脱氧葡萄糖标记的葡萄糖摄取、Western–blot检测葡萄糖转运因子4(GLUT4)蛋白表达、实时荧光定量逆转录多聚酶联反应(RT–qPCR)检测肿瘤坏死因子α(TNF–α)、白细胞介素6(IL–6)、C反应蛋白(CRP)mRNA 表达,酶标记免疫吸附测定法(ELISA)检测培养液中TNF–α 、IL–6、CRP 蛋白含量。
      结果  与对照组比较,模型组脂肪细胞葡萄糖摄取和GLUT4蛋白表达明显降低(P < 0.05),TNF–α、IL–6、CRP mRNA明显升高(P < 0.01),TNF–α、IL–6、CRP蛋白分泌量分别为(161.3 ± 14.2)、(121.6 ± 13.6)、(1.82 ± 0.17)明显升高(P < 0.01);与模型组比较,EGCG组脂肪细胞葡萄糖摄取和GLUT4蛋白表达明显增加(P < 0.05),TNF–α、IL–6、CRP mRNA明显下降(P < 0.01),低、中、高剂量EGCG组脂肪细胞TNF–α、IL–6、CRP蛋白分泌量分别为(148.8 ± 13.3)、(93.3 ± 10.4)、(1.74 ± 0.12)pg/mL,(131.4 ± 11.3)、(85.5 ± 14.1)、(1.53 ± 0.15)pg/mL和(119.5 ± 12.1)、(73.9 ± 11.3)、(1.36 ± 0.12)pg/mL明显降低(P < 0.01),呈剂量效应关系。
      结论  EGCG可促进脂肪细胞葡萄糖摄取和增强胰岛素敏感性,进而改善胰岛素抵抗,其机制可能与降低脂肪细胞炎症因子表达有关。

     

    Abstract:
      Objective  To observe the effect of phytochemicals-epigallocatechin gallate (EGCG) on the expression of glucose transporter, insulin sensitivity and inflammatory factors in SW872 adipocytes with insulin resistance (IR).
      Methods  The insulin resistance model of SW872 adipocytes was constructed with oleic acid then the adipocytes were treated with EGCG at different doses (25, 50, and 100 μmol/L) for 24 hours. The uptake of 2-deoxy glucose labeled glucose of the adipocytes was detected with confocal laser scanning microscopy. The expression of glucose transporter type 4 (GLUT4) protein was determined with Westernblot. The mRNA expressions of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP) were detected with real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-qPCR) and the expressions of TNF-α, IL-6, and CRP protein were measured with enzyme-linked immunosorbent assay (ELISA).
      Results  Compared with those of the control cells, the glucose uptake and the expression of GLUT4 protein of the model cells were significantly decreased (both P < 0.05), and the levels of TNF-α, IL-6, CRP mRNA expression were significantly increased (all P < 0.01). The protein secretion of TNF-α (161.3 ± 14.2 pg/mL), IL-6 (121.6 ± 13.6 pg/mL), and CRP (1.82 ± 0.17 pg/mL) in the model cells were also significantly higher than those in the control cells (P < 0.01 for all). In EGCG treated adipocytes, the glucose uptake and GLUT4 protein increased significantly (both P < 0.05), while the mRNA expressions of TNF-α, IL-6, and CRP decreased significantly (P < 0.01 for all) compared with those in the model cells. In the SW872 adipocytes treated with high, moderate, and low dose EGCG, the protein expressions of TNF-α (148.8 ± 13.3, 131.4 ± 11.3, and 119.5 ± 12.1 pg/mL), IL-6 (93.3 ± 10.4, 85.5 ± 14.1, and 73.9 ± 11.3 pg/mL), and CRP (1.74 ± 0.12, 1.53 ± 0.15, and 1.36 ± 0.12 pg/mL) were significantly reduced in a dose dependent manner compared with those in the model cells (P < 0.01 for all).
      Conclusion  EGCG can promote glucose uptake and enhance insulin sensitivity, thereby improving insulin resistance; the mechanism of the effects may be related to the reduction in inflammatory factor expression.

     

/

返回文章
返回