Suppressive effect of ursodeoxycholic acid on type IIA phospholipase A2 expression in HepG2 cells.
Suppressive effect of ursodeoxycholic acid on type IIA phospholipase A2 expression in HepG2 cells.
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熊去氧胆酸对 HepG2 细胞中 IIA 型磷脂酶 A2 表达的抑制作用。
DOI：
10.1002/hep.20630
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Tanaka,Naomi
中科院分区：
文献类型：
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作者：
Ikegami,Tadashi;Matsuzaki,Yasushi;Fukushima,Sugano;Shoda,Junichi;Olivier,JeanLuc;Bouscarel,Bernard;Tanaka,Naomi
磷脂酶A2 IIA（PLA 2 IIA）在花生四烯酸代谢和炎症中起关键作用，在各种病理条件下上调，包括在患有多发性胆固醇结石的患者的胆囊和胆囊胆汁中，在患有肝硬化的大鼠的肝脏和肾脏中，以及在用化学致癌物处理的动物的结肠组织中。熊去氧胆酸（UDCA）给药部分减弱了这些不同模型中的PLA 2 IIA表达水平。本研究的目的是在细胞水平上研究UDCA对PLA 2 IIA表达水平的调节作用。以HepG 2细胞为研究对象，观察UDCA对PLA 2 IIA表达水平的直接抑制作用。UDCA以剂量依赖性方式部分抑制HepG 2细胞中促炎细胞因子（白细胞介素-6和肿瘤坏死因子α）诱导的PLA 2 IIA表达。UDCA对促炎细胞因子诱导的PLA 2 IIA表达的影响发生在转录水平。此外，在检测的胆汁酸中，这种抑制作用是UDCA特异性的。总之，本研究支持花生四烯酸代谢和PLA 2 IIA表达水平的可能改变，特别是UDCA在慢性肝病患者中的保护作用。（肝脏病学2005;41：896-905。）
Phospholipase A2IIA (PLA2IIA), which plays a crucial role in arachidonic acid metabolism and in inflammation, is upregulated under various pathological conditions, including in the gallbladder and gallbladder bile from patients with multiple cholesterol gallstones, in the liver and kidney of rats with cirrhosis, as well as in the colonic tissue of animals treated with a chemical carcinogen. The administration of ursodeoxycholic acid (UDCA) partially attenuated the PLA2IIA expression level in these different models. The aim of this study was to investigate the modulatory effect of UDCA on the PLA2IIA expression level at the cellular level. The HepG2 cells were selected to investigate the direct inhibitory effect of UDCA on PLA2IIA expression level. The proinflammatory cytokines (interleukin‐6 and tumor necrosis factor α) ‐induced PLA2IIA expression in HepG2 cells was partially inhibited by the presence of UDCA in a dose‐dependent fashion. The effect of UDCA on proinflammatory cytokines‐induced PLA2IIA expression occurred at the transcriptional level. In addition, among the bile acids tested, this inhibitory effect was UDCA‐specific.In conclusion, this study supports the possible alteration of arachidonic acid metabolism and PLA2IIA expression level, in particular, as the protective action of UDCA in patients with chronic liver disease. (HEPATOLOGY2005;41:896–905.)