Nishigaki Y, Ohnishi H, Moriwaki H, Muto Y
First Department of Internal Medicine, Gifu University School of Medicine, Japan.
Dig Dis Sci. 1996 Jul;41(7):1487-93. doi: 10.1007/BF02088577.
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 E2 concentration in culture supernatants of lymphocytes from healthy volunteers to a lower level than that in culture incubated with chenodeoxycholic acid (P < 0.05) or control cultures (P < 0.01). Urosdeoxycholic acid normalized the defective natural killer activity in primary biliary cirrhosis by reducing the levels of other hydrophobic bile acids and inhibiting prostaglandin E2 production, suggesting that it may be a useful immunomodulating agent for primary biliary cirrhosis.
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活性缺陷的影响。给予熊去氧胆酸（每日600毫克）为期一个月显著提高了原发性胆汁性肝硬化患者的自然杀伤活性（P < 0.05）。熊去氧胆酸还增强了健康志愿者淋巴细胞的体外自然杀伤活性，而其他疏水性胆汁酸则降低了该活性。此外，熊去氧胆酸将健康志愿者淋巴细胞培养上清液中的前列腺素E2浓度降低至低于与鹅去氧胆酸共同培养（P < 0.05）或对照培养（P < 0.01）时的水平。熊去氧胆酸通过降低其他疏水性胆汁酸水平并抑制前列腺素E2生成，使原发性胆汁性肝硬化患者缺陷的自然杀伤活性恢复正常，这表明它可能是一种用于原发性胆汁性肝硬化的有用免疫调节剂。
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