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目的探讨黄芪多糖对3T3-L1脂肪细胞脂联素的分泌及其mRNA表达的影响。方法3T3-L1脂肪细胞促分化成熟后,给予不同质量浓度的黄芪多糖(APS)(0.001、0.010、0.100、1.000g/L)干预48h,收集其细胞和培养上清液,采用酶联免疫吸附试验(ELISA)检测细胞上清液脂联素水平,半定量反转录聚合酶链反应(RT-PCR)检测脂肪细胞脂联素和过氧化物酶体增殖物激活型受体γ(PPARγ)mRNA表达水平。采用SPSS13.0软件进行统计学分析。结果体外培养的3T3-L1脂肪细胞在地塞米松、胰岛素和三碘甲腺原氨酸的作用下能成功分化为成熟的脂肪细胞。与对照组比较,0.100g/L黄芪多糖组可使脂联素分泌及其mRNA表达显著增加(P<0.001),而0.001g/L黄芪多糖则降低脂联素的分泌(P<0.001)。0.100g/L黄芪多糖组PPARγ mRNA表达亦显著增加(P<0.01),1.000g/L黄芪多糖使3T3-L1脂肪细胞脂联素分泌及其mRNA表达显著减少(P<0.01),PPARγ mRNA表达无明显改变(P>0.05)。结论黄芪多糖可促进3T3-L1脂肪细胞脂联素分泌及其mRNA表达,活化PPARγ mRNA的表达,这可能是体内黄芪多糖改善胰岛素抵抗的途径之一。
Objective To investigate the effect of astragalus polysaccharides on the secretion and mRNA expression of adiponectin in 3T3-L1 adipocytes. Methods 3T3-L1 adipocytes were differentiated and matured, and then treated with different concentrations of APS (0.001, 0.010, 0.100, 1.000 g/L) for 48 hours. Cells and culture supernatants were collected and used for enzyme-linked immunosorbent assay (ELISA). Adiponectin levels in cell supernatants were measured by ELISA, and adiponectin and peroxisome proliferator-activated receptor γ (PPARγ) were detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). mRNA expression level. SPSS13.0 software was used for statistical analysis. Results The 3T3-L1 adipocytes cultured in vitro successfully differentiated into mature adipocytes under the action of dexamethasone, insulin and triiodothyronine. Compared with the control group, the 0.100 g/L astragalus polysaccharide group significantly increased adiponectin secretion and mRNA expression (P<0.001), while 0.001 g/L astragalus polysaccharide decreased adiponectin secretion (P<0.001). The expression of PPARγ mRNA was also significantly increased in 0.100 g/L astragalus polysaccharide group (P<0.01), and the adiponectin secretion and mRNA expression in 3T3-L1 adipocytes was significantly decreased (P<0.01) and 1.000 g/L astragalus polysaccharide expression. No significant change (P>0.05). Conclusion Astragalus polysaccharides can promote the secretion and mRNA expression of adiponectin in 3T3-L1 adipocytes and activate the expression of PPARγ mRNA, which may be one of the ways to improve insulin resistance in vivo.