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目的观察阿托伐他汀对氧化型低密度脂蛋白(oxLDL)刺激下3T3-L1脂肪细胞分泌功能的影响,并探讨其作用机制。方法 3T3-L1脂肪细胞促分化成熟后,oxLDL刺激脂肪细胞,给予不同浓度的阿托伐他汀干预,收集细胞,测定脂肪细胞肿瘤坏死因子-α(TNF-α)浓度、TNF-α和PPAR-γmRNA表达水平及核因子-κB(NF-κB)活性。结果 oxLDL刺激使3T3-L1脂肪细胞分泌TNF-α、TNF-αmRNA表达水平明显增高。阿托伐他汀呈浓度依赖性抑制oxLDL刺激下TNF-α分泌、TNF-αmRNA表达和NF-κB活化,并增强PPAR-γmRNA表达。1.0及10.0μM阿托伐他汀干预组TNF-α水平、TNF-αmRNA表达低于oxLDL刺激组(P<0.05),10.0μM阿托伐他汀干预组PPAR-γmRNA表达高于oxLDL组,NF-κB活性低于oxLDL刺激组(P<0.05);TNF-α水平、TNF-αmRNA表达、NF-κB活性和PPAR-γmRNA表达10.0和0.1μM阿托伐他汀干预组比较差异均有统计学意义(P<0.05)。结论阿托伐他汀能抑制ox-LDL刺激下3T3-L1脂肪细胞TNF-α分泌、TNF-αmRNA表达和NF-κB活性,增强PPAR-γmRNA表达,PPAR-γ与NF-κB可能介导了他汀类药物对脂肪细胞炎性过程的调节。
Objective To observe the effect of atorvastatin on the secretory function of 3T3-L1 adipocytes stimulated by oxLDL, and to explore its mechanism. Methods After promoting the differentiation of 3T3-L1 adipocytes, oxLDL stimulated adipocytes and treated with different concentrations of atorvastatin. The cells were collected and the concentrations of tumor necrosis factor-α (TNF-α), TNF-α and PPAR- γ mRNA expression and nuclear factor-κB (NF-κB) activity. Results OxLDL stimulated TNF-α and TNF-α mRNA expression in 3T3-L1 adipocytes. Atorvastatin inhibited the secretion of TNF-α, TNF-αmRNA and NF-κB, and enhanced the expression of PPAR-γmRNA in oxLDL-stimulated cells in a concentration-dependent manner. The levels of TNF-α and TNF-αmRNA in 1.0 and 10.0μM atorvastatin intervention groups were lower than those in oxLDL stimulation groups (P <0.05). The expression of PPAR-γmRNA in 10.0μM atorvastatin group was higher than that in oxLDL group and NF-κB (P <0.05). The levels of TNF-α, TNF-αmRNA, NF-κB activity and PPAR-γmRNA expression were significantly lower in the 10.0 and 0.1μM atorvastatin intervention groups than in the oxLDL stimulation group (P <0.05) <0.05). Conclusions Atorvastatin can inhibit the secretion of TNF-α, TNF-αmRNA and NF-κB in 3T3-L1 adipocytes stimulated by ox-LDL, and enhance the expression of PPAR-γmRNA. PPAR-γ and NF-κB may mediate statin Regulatory effect of drugs on the inflammatory process of adipocytes.