Suppressive effect of ursodeoxycholic acid on type IIA phospholipase A2 expression in HepG2 cells.

磷脂酶A（2）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，包括在多发性胆固醇结石患者的胆囊和胆囊胆汁中，在肝硬化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PLA（2）IIA的表达水平。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，这种抑制作用具有UDCA特异性。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对慢性肝病患者的保护作用。

Phospholipase A(2) IIA (PLA(2)IIA), 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 PLA(2)IIA expression level in these different models. The aim of this study was to investigate the modulatory effect of UDCA on the PLA(2)IIA expression level at the cellular level. The HepG2 cells were selected to investigate the direct inhibitory effect of UDCA on PLA(2)IIA expression level. The proinflammatory cytokines (interleukin-6 and tumor necrosis factor alpha)-induced PLA(2)IIA 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 PLA(2)IIA 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 PLA(2)IIA expression level, in particular, as the protective action of UDCA in patients with chronic liver disease.