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目的观察表没食子儿茶素没食子酸酯(EGCG)对脂多糖(LPS)处理的THP-1源性泡沫细胞胆固醇流出及其ABCA1活性的影响,并探讨其机制。方法建立THP-1源性泡沫细胞模型,加入不同浓度LPS进行炎性刺激。在LPS刺激前1 h,加入不同浓度EGCG预处理。MTT法检测EGCG处理后细胞存活性。油红O染色观察细胞脂质蓄积。高效液相色谱法检测细胞胆固醇流出水平。实时定量PCR和Western blot法检测细胞内mRNA和蛋白质水平。EMSA检测细胞NF-κB活性。结果 EGCG预处理对细胞存活率不产生影响。不同浓度LPS处理细胞后,脂质蓄积增多胆固醇流出减少,而EGCG预处理减轻了脂质蓄积并且增加胆固醇流出率。LPS处理能够抑制细胞内ABCA1 mRNA和蛋白水平,而EGCG预处理能够显著衰弱LPS的抑制作用。LPS刺激后NF-κB活性增加,而EGCG预处理能够降低LPS诱导的NF-κB活性。结论 EGCG能够通过抑制NF-κB活性,来降低LPS对THP-1源性泡沫细胞ABCA1的抑制作用,促进细胞内胆固醇的流出。
Objective To observe the effects of epigallocatechin gallate (EGCG) on cholesterol efflux and ABCA1 activity in lipopolysaccharide (LPS) -treated THP-1-derived foam cells and to explore its mechanism. Methods THP-1 derived foam cell model was established, and different concentrations of LPS were added for inflammatory stimulation. One hour before LPS stimulation, different concentrations of EGCG were added to pretreat. Cell viability was detected by MTT assay after EGCG treatment. Oil red O staining observed cell lipid accumulation. High-performance liquid chromatography was used to detect the level of cellular cholesterol efflux. Real-time quantitative PCR and Western blot were used to detect intracellular mRNA and protein levels. EMSA detection of NF-κB activity. Results EGCG pretreatment did not affect cell viability. Lipid accumulation increased cholesterol efflux after treatment with different concentrations of LPS, whereas EGCG pretreatment reduced lipid accumulation and increased cholesterol efflux. LPS treatment can inhibit intracellular ABCA1 mRNA and protein levels, while EGCG pretreatment can significantly weaken the inhibitory effect of LPS. NF-κB activity increased after LPS stimulation, while EGCG pretreatment could reduce LPS-induced NF-κB activity. Conclusion EGCG can inhibit the inhibitory effect of LPS on ABCA1 in THP-1-derived foam cells by inhibiting the activity of NF-κB, and promote the efflux of intracellular cholesterol.