黄芩苷对氧化低密度脂蛋白诱导的血管内皮细胞凋亡的防护作用

目的：研究黄芩苷抑制氧化低密度脂蛋白（oxLDL）诱导的血管内皮细胞凋亡及其介导机制。方法：应用大鼠模型，以低密度脂蛋白（LDL）体内诱导血管内皮细胞凋亡，并以黄芩苷进行干预，观察其对LDL诱导血管内皮细胞凋亡的影响。原位末端标记技术（TUNEL）法检测凋亡细胞，比色法测半胱天冬蛋白酶3（Caspase-3）的活性。结果：LDL组与氯化钠对照组比较，血管内皮细胞凋亡数显著增加，caspase-3酶活性显著增高，黄芩苷干预组与LDL组比较，凋亡细胞数显著减少，caspase-3酶活性下降。结论：LDL可能通过激活caspase-3使大鼠血管内皮细胞凋亡；黄芩苷可通过抑制caspase-3酶活性抑制LDL诱导的细胞凋亡。

Protective Effect of Baicalin on Apoptosis of Vascular Endothelial Cells Induced by Oxidized Low Density Lipoprotein

Objective：To research the inhibitive effect and mechanism of baicalin on apoptosis of vascular endothelial cells in rats induced by oxidized low density lipoprotein （ox-LDL）. Methods：The rats were firstly intravenously injected with LDL, then intervened by baicalin to be observed for any changes, and compared with rats treated with NaCl2 only, and rats treated with LDL but without baicalin intervention. Apoptosis were detected by TUNEL method, activity of caspase-3 enzyme was assayed by colorimetric assay. Results： Compared with NaCl2 only rats, the LDL group showed larger number of apoptosis cells, and caspase-3 with higher activity （P 〈 0.01 ） which were inhibited significantly by baicalin as shown in the intervention group （P 〈 0.01 ）. Conclusion： LDL stimulates activity of caspase-3 to cause apoptosis of vascular endothelial cells; baicalin can inhibit such apopotosis by restricting activity of caspase-3.