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目的探讨黄芩苷对脂质运载蛋白-2(LCN-2)诱导人脐静脉内皮细胞(HUVEC)损伤的保护作用及其可能机制。方法以脂质运载蛋白-2不同浓度(0、5、10、20μmol·L-1)和不同时间(0、24、48、72 h)作用人脐静脉内皮细胞,检测人脐静脉内皮细胞增殖、凋亡、细胞上清液中白细胞介素-6(IL-6)及单核细胞趋化蛋白-1(MCP-1)水平及乳酸脱氢酶(LDH)活性、细胞内p-JNK、Bax、Bcl-2蛋白表达,分别加入不同质量浓度黄芩苷(15、30、60 mg·L~(-1))和JNK通路特异性阻滞剂SP600125 10μmol·L-1检测黄芩苷的干预作用及机制。结果与对照组比较,10μmol·L-1脂质运载蛋白-2可显著抑制人脐静脉内皮细胞增殖,上调人脐静脉内皮细胞内p-JNK蛋白表达及Bax/Bcl-2蛋白比率以促进人脐静脉内皮细胞凋亡、诱导人脐静脉内皮细胞分泌白细胞介素-6及单核细胞趋化蛋白-1、增加乳酸脱氢酶活性(P<0.05);与脂质运载蛋白-2组比较,30 mg·L~(-1)黄芩苷可显著减轻脂质运载蛋白-2诱导的人脐静脉内皮细胞增殖抑制、下调人脐静脉内皮细胞内p-JNK蛋白表达及Bax/Bcl-2蛋白比率以抑制人脐静脉内皮细胞凋亡、减少脂质运载蛋白-2诱导人脐静脉内皮细胞分泌IL-6及单核细胞趋化蛋白-1、降低乳酸脱氢酶活性(P<0.05)。结论黄芩苷可通过抑制JNK通路,减轻脂质运载蛋白-2诱导的人脐静脉内皮细胞损伤。
Objective To investigate the protective effect of baicalin on the injury of human umbilical vein endothelial cells (HUVEC) induced by lipoxygenin-2 (LCN-2) and its possible mechanism. Methods Human umbilical vein endothelial cells (HUVECs) were treated with different concentrations of lipocalin-2 (0, 5, 10, 20 μmol·L-1) and different time periods (0, 24, 48, 72 h) , Apoptosis, interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) and lactate dehydrogenase (LDH) Bax and Bcl-2 protein were detected and the effects of different concentrations of baicalin (15, 30, 60 mg · L -1) and SP600125 10 μmol·L -1 JNK specific blocker And mechanism. Results Compared with the control group, 10μmol·L-1 lipocalin-2 could significantly inhibit the proliferation of human umbilical vein endothelial cells and up-regulate the expression of p-JNK protein and Bax / Bcl-2 protein in human umbilical vein endothelial cells The apoptosis of human umbilical vein endothelial cells induced the secretion of interleukin-6 and monocyte chemoattractant protein-1 in human umbilical vein endothelial cells and increased the activity of lactate dehydrogenase (P <0.05). Compared with the lipoxygenase-2 group , Baicalin at a dose of 30 mg · L -1 could significantly reduce the inhibitory effect of CCL-2 on the proliferation of human umbilical vein endothelial cells and down-regulate the expression of p-JNK protein and Bax / Bcl-2 protein in human umbilical vein endothelial cells Ratio to inhibit the apoptosis of human umbilical vein endothelial cells and decrease the secretion of IL-6 and monocyte chemoattractant protein-1 by lipocalin-2 and decrease the activity of lactate dehydrogenase (P <0.05). Conclusion Baicalin can reduce the injury of human umbilical vein endothelial cells induced by lipocalin-2 by inhibiting the JNK pathway.