目的 从c-Jun氨基末端激酶（JNK）信号通路研究黄芩苷对乙酰化低密度脂蛋白（acetylate low-density lipoprotein，AcLDL）联合脂多糖 （lipopolysaccharide，LPS）诱导的与动脉粥样硬化（atherosclerosis，AS）相关巨噬细胞凋亡的影响。方法 收集小鼠腹腔巨噬细胞RAW 264.7进行体外培养，以100 μg ·mL-1的AcLDL及1 μg·mL-1的LPS诱导巨噬细胞凋亡作为模型组，用黄芩苷低、中、高剂量组（120，240，480 μg·mL-1）进行干预，Annexin-V和PI双染后用流式细胞仪 检测细胞凋亡，Western-blot技术检测JNK蛋白表达及实时荧光定量PCR技术检测JNK mRNA表达。结果 AcLDL对照组、LPS对照组、AcLDL+LPS模型组与正常组比较，差异有统 计学意义（P ＜ 0.01），Ac-LDL+LPS模型组细胞凋亡率明显高于正常组。黄芩苷中、高剂量组细胞凋亡率明显高于AcLDL+LPS模型组，差异有统计学意义（P ＜ 0.05，P ＜ 0.01）。AcLDL+LPS联合干预较AcLDL或LPS单独干预引起的磷酸化JNK高，随着黄芩苷干预剂量的增高，磷酸化JNK表达有升高的趋势。结论 脂多糖和乙酰化低密度脂蛋白双 重打击是诱导巨噬细胞凋亡的重要原因，JNK信号通路参与这一过程。黄芩苷可能通过增强磷酸化JNK表达来促进脂多糖和乙酰化低密度脂蛋白诱导的巨噬细胞早期凋亡，从 而拮抗早期动脉粥样硬化的病理进程。

Objective To study the effect of baicalin on macrophages apoptosis associated with atherosclerosis（AS）induced by acetylated low-density lipoprotein（AcLDL） and lipopolysaccharide（LPS） from the JNK signaling pathway. Methods Macrophages were harvested from the peritonea of mice，and then 100 μg/mL of AcLDL and 1 μg/mL of LPS were used for inducing macrophages apoptosis. After intervention with 120，240，and 480 μg/mL of baicalin，Western blot and quantitative RT-PCR were used to determine the expression of JNK，and the apoptotic rate of macrophages was detected with flow cytometry（FCM） after the staining of Annexin-V and PI. Results The apoptotic rate of macrophages in AcLDL group，LPS group，and AcLDL+LPS group differed from that in the normal group，and was much higher in AcLDL+LPS group（P＜0.01）. High- and middle-dose baicalin groups had higher apoptotic rate than that in AcLDL+LPS group（P＜0.01）. The expression of phosphorylated JNK caused by AcLDL+LPS was higher than that caused by AcLDL or LPS alone. With the increase of baicalin dose，phosphorylated JNK expression increased gradually. Conclusion AcLDL and LPS are the important reason for macrophage apoptosis，and the JNK signaling pathway is involved in this process. The mechanism of baicalin for promoting the early apoptosis of macrophages induced by AcLDL and LPS is probably related with the enhancement of JNK activity，thus baicalin can counteract the pathological process of the early atherosclerosis.

R285.5

广东省自然科学基金资助项目（s2012010008193）。