Ursodeoxycholic acid corrects defective natural killer activity by inhibiting prostaglandin E(2) production in primary biliary cirrhosis
Ursodeoxycholic acid corrects defective natural killer activity by inhibiting prostaglandin E(2) production in primary biliary cirrhosis
复制标题
DOI：
10.1007/bf02088577
复制
发表时间：
1996-07-01
影响因子：
3.1
通讯作者：
Muto, Y
中科院分区：
文献类型：
--
作者：
Nishigaki, Y;Ohnishi, H;Muto, Y
我们评估了熊去氧胆酸对原发性胆汁性肝硬化患者自然杀伤细胞活性缺陷的影响。熊去氧胆酸600 mg/d治疗1个月后，原发性胆汁性肝硬化患者的自然杀伤细胞活性明显升高（P < 0.05）。熊去氧胆酸还能增强健康人淋巴细胞的体外自然杀伤活性，而其它疏水性胆汁酸则能抑制这种活性。此外，熊去氧胆酸还能降低健康人淋巴细胞培养上清中前列腺素E（2）的浓度，使其低于鹅去氧胆酸（P < 0.05）或对照培养上清中前列腺素E（2）的浓度（P < 0.01）。熊去氧胆酸通过降低其他疏水性胆汁酸的水平和抑制前列腺素E（2）的产生，使原发性胆汁性肝硬化中缺陷的自然杀伤活性正常化，这表明熊去氧胆酸可能是原发性胆汁性肝硬化有用的免疫调节剂。
We evaluated the effect of ursodeoxycholic acid on the defective natural killer activity in primary biliary cirrhosis. Administration of ursodeoxycholic acid (600 mg daily) for one month significantly increased natural killer activity in patients with primary biliary cirrhosis (P < 0.05). Ursodeoxycholic acid also enhanced the in vitro natural killer activity of lymphocytes from healthy volunteers, while other hydrophobic bile acids depressed it, Furthermore, ursodeoxycholic acid reduced the prostaglandin E(2) concentration in culture supernatants of lymphocytes from healthy volunteers to a lower level than that in cultures incubated with chenodeoxycholic acid (P < 0.05) or control cultures (P < 0.01). Ursodeoxycholic acid normalized the defective natural killer activity in primary biliary cirrhosis by reducing the levels of other hydrophobic bile acids and inhibiting prostaglandin E(2) production, suggesting that it may be a useful immunomodulating agent for primary biliary cirrhosis.