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目的探讨川芎嗪对氧化低密度脂蛋白(ox-LDL)诱导内皮细胞炎症反应的影响及其分子机制。方法体外培养的人冠状动脉内皮细胞,随机分为正常对照组(无干预)、ox-LDL组(50mg/Lox-LDL)、川芎嗪组(1、10、100μmol/L川芎嗪+50mg/Lox-LDL),观察川芎嗪对细胞间黏附分子1(ICAM-1)和环氧酶2基因和蛋白表达的影响;进一步检测与其耦联的p38丝裂原活化蛋白激酶(p38MAPK)和核转录因子κB(NF-κB)信号通路活化的影响。结果与ox-LDL组比较,川芎嗪(10、100μmol/L)降低ICAM-1的基因表达(1.49±0.26、1.81±0.05比2.36±0.34,P<0.01),抑制环氧酶2的蛋白表达(0.21±0.03、0.13±0.04比0.48±0.01,P<0.05);川芎嗪(1、10μmol/L)降低ICAM-1的蛋白表达(0.16±0.03、0.14±0.02比0.87±0.05),抑制上述黏附分子和炎症因子耦联的信号分子p38MAPK的磷酸化激活(0.30±0.10、0.12±0.06比0.66±0.15),抑制信号分子NF-κB蛋白(0.32±0.08、0.20±0.11比0.62±0.10)表达水平的升高(均P<0.01)。结论川芎嗪具有对抗ox-LDL诱导的内皮细胞炎症和黏附反应,并抑制MAPK和NF-κB信号通路的激活。
Objective To investigate the effect of ligustrazine on endothelial cell inflammation induced by ox-LDL and its molecular mechanism. Methods Human coronary artery endothelial cells cultured in vitro were randomly divided into normal control group (no intervention), ox-LDL group (50mg / Lox-LDL), ligustrazine group (1,10,100μmol / L Ligustrazine + 50mg / Lox -LDL) was used to observe the effect of ligustrazine on the expression of ICAM-1 and cyclooxygenase 2 gene and protein. The expression of p38 mitogen-activated protein kinase (p38MAPK) and nuclear transcription factor κB (NF-κB) signaling pathway activation. Results Compared with ox-LDL group, ligustrazine (10,100 μmol / L) decreased the expression of ICAM-1 gene (1.49 ± 0.26, 1.81 ± 0.05 vs 2.36 ± 0.34, P <0.01) (0.21 ± 0.03,0.13 ± 0.04 vs 0.48 ± 0.01, P <0.05). Ligustrazine (1,10μmol / L) decreased the protein expression of ICAM-1 (0.16 ± 0.03,0.14 ± 0.02 vs 0.87 ± 0.05) The phosphorylation of p38 MAPK (0.30 ± 0.10, 0.12 ± 0.06 vs 0.66 ± 0.15) and the expression of NF-κB (0.32 ± 0.08, 0.20 ± 0.11 vs. 0.62 ± 0.10) were both inhibited by adhesion molecules and inflammatory cytokines (All P <0.01). Conclusion Tetramethylpyrazine can antagonize ox-LDL-induced endothelial cell inflammation and adhesion reaction, and inhibit the activation of MAPK and NF-κB signaling pathway.