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目的:研究大黄素、小檗碱对具有胰岛素抵抗的HepG2细胞的治疗作用及其机制。方法:用MTT法筛选大黄素、小檗碱作用于HepG2细胞的实验浓度,然后用游离脂肪酸诱导HepG2细胞使其成为具有胰岛素抵抗的细胞作为模型组,在模型组中分别给予大黄素、小檗碱、地塞米松进行干预,通过葡萄糖氧化酶、蒽酮法、RT-PCR法检测细胞上糖代谢及瘦素长型受体、短型受体mRNA的表达水平。结果:大黄素、小檗碱、地塞米松组培养液中葡萄糖含量及细胞内糖原含量较模型组明显改善,细胞上瘦素长型及短型受体mRNA的水平明显上调,较正常组无明显改变。结论:大黄素、小檗碱均能增加葡萄糖的消耗,增加细胞内糖原含量,上调瘦素受体mRNA的表达水平,表示它们可通过调节糖代谢及瘦素受体的表达水平来治疗胰岛素抵抗。
Objective: To study the therapeutic effect and mechanism of emodin and berberine on HepG2 cells with insulin resistance. METHODS: The experimental concentration of emodin and berberine in HepG2 cells was screened by MTT assay, and HepG2 cells were induced to become insulin resistant cells using the free fatty acids as a model group, and emodin and picolinol were administered to the model group, respectively. Alkaline and dexamethasone were used to intervene. Glucose oxidase, anthrone method, and RT-PCR were used to detect the glucose metabolism and leptin long receptor and short receptor mRNA expression. Results: Compared with the model group, glucose content and intracellular glycogen content in emodin, berberine, and dexamethasone groups were significantly improved compared with the model group. The mRNA levels of long and short receptors on leptin in the cells were significantly increased compared with the normal group. No significant change. CONCLUSION: Both emodin and berberine can increase glucose consumption, increase intracellular glycogen content, and upregulate leptin receptor mRNA expression, indicating that they can treat insulin by regulating glucose metabolism and expression of leptin receptors. resistance.