Hydroxysafflor yellow A protects methylglyoxal-induced injury in the cultured human brain microvascular endothelial cells
Hydroxysafflor yellow A protects methylglyoxal-induced injury in the cultured human brain microvascular endothelial cells
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羟基红花黄A保护甲基乙二醛诱导的人脑微血管内皮细胞损伤
DOI：
10.1016/j.neulet.2013.06.007
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发表时间：
2013-08-09
影响因子：
2.5
通讯作者：
Dai, Haibin
中科院分区：
文献类型：
--
作者：
Li, Wenlu;Liu, Jie;Dai, Haibin
糖尿病患者体内存在高浓度的甲基乙二醛（MGO），并具有晚期糖基化终产物（AGES），其在血管并发症（如中风）中起重要作用。我们的前期研究表明，红花黄色素的主要活性成分羟基红花黄色素A（HSYA）在体外对AGES的形成具有抗糖化作用。目前尚不清楚HSYA是否能保护培养的人脑微血管内皮细胞（HBMEC）免受MGO诱导的损伤。使用培养的HBMEC，通过3-（4，5-二甲基噻唑-2-基）-2，5-二苯基溴化四氮唑（MU）形成、乳酸脱氢酶（LDH）释放和AnnexinV/PI染色来测量细胞损伤。通过Western印迹法测定晚期糖原终产物和caspase-3的形成。HSYA（10 ~ 100 μ mol/l）可明显抑制MGO对HBMEC的损伤作用。Caspase-3表达和AnnexinV/PI染色结果表明HSYA的保护作用可能与抑制细胞凋亡有关。此外，MGO还能促进HBMEC中AGEs的积累，100 μ mol/l HSYA也能抑制AGEs的积累。因此，我们的研究结果表明，HSYA可以抑制MGO诱导的HBMEC损伤，这与其抗糖基化作用有关。(C)2013爱思唯尔爱尔兰有限公司版权所有。
Individuals with diabetes have high concentration of methylglyoxal (MGO) and have advanced glycation end-products (AGES) which play an important role in vascular complications, such as stroke. Our previous data demonstrated that hydroxysafflor yellow A (HSYA), a major active chemical component of the safflower yellow pigment, had antiglycation effect on the AGES formation in vitro. It is not known whether HSYA can protect against MGO-induced injury in cultured human brain microvascular endothelial cells (HBMEC). Using cultured HBMEC, cell injury was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MU) formation, lactate dehydrogenase (LDH) release and AnnexinV/PI staining. Advanced glycogen end-products and caspase-3 formation were measured by Western blotting. Incubation of MGO for 24 h concentration-dependently induced HBMEC injury, which was protected by HSYA from 10 to 100 mu mol/l. Caspase-3 expression and AnnexinV/PI staining illustrated that the protection of HSYA was probably associated with inhibiting cell apoptosis. What's more, MGO promoted AGEs accumulation in the cultured HBMEC, which was also inhibited by 100 mu mol/l HSYA. Thus, our results proved that HSYA could inhibit MGO-induced injury in the cultured HBMEC, which was associated with its antiglycation effect. (C) 2013 Elsevier Ireland Ltd. All rights reserved.