Balkan Jale, Parldar Fatma Hande, Doğru-Abbasoğlu Semra, Aykaç-Toker Gülçin, Uysal Müjdat
Department of Biochemistry, Istanbul Faculty of Medicine, Istanbul University, Capa 34093 Istanbul, Turkey.
Eur J Gastroenterol Hepatol. 2005 Sep;17(9):917-21. doi: 10.1097/00042737-200509000-00006.
Taurine or betaine have been reported to have antioxidative potential and inhibit Kupffer cell activation. These effects may play an important role in their hepatoprotective effects. Therefore, they may also have protective effects in lipopolysaccharide hepatotoxicity by both inhibiting Kupffer cell activation and behaving as antioxidants.
The prophylactic efficiency of taurine or betaine pretreatment for the prevention of peroxidative changes induced by lipopolysaccharide treatment in the rat liver was investigated.
Lipopolysaccharide (10 mg/kg intraperitoneally) was given to rats pretreated with taurine (1.5%, w/v) or betaine (1.5%, w/v) in drinking water for 4 weeks and plasma transaminase activities as well as hepatic malondialdehyde, diene conjugate (DC), glutathione, alpha-tocopherol and ascorbic acid levels, and superoxide dismutase (SOD) and glutathione peroxidase activities were determined.
Significant increases in plasma transaminase activities and hepatic malondialdehyde and DC levels and decreases in hepatic glutathione and alpha-tocopherol levels and SOD and glutathione peroxidase activities were observed 6 h after lipopolysaccharide treatment. This treatment did not alter ascorbic acid levels in the liver compared with controls. Taurine or betaine pretreatment in lipopolysaccharide-injected rats caused significant decreases in plasma transaminase activities and hepatic malondialdehyde and DC levels, and significant increases in glutathione and alpha-tocopherol (not betaine) levels without changing ascorbic acid levels and SOD and glutathione peroxidase activities in the liver.
Our findings clearly indicate that taurine or betaine pretreatment was effective in the prevention of lipopolysaccharide-induced hepatotoxicity and prooxidant status.
据报道，牛磺酸或甜菜碱具有抗氧化潜力并能抑制库普弗细胞活化。这些作用可能在其肝脏保护作用中发挥重要作用。因此，它们可能通过抑制库普弗细胞活化和作为抗氧化剂，对脂多糖肝毒性也具有保护作用。
研究了牛磺酸或甜菜碱预处理对预防大鼠肝脏中脂多糖处理诱导的过氧化变化的预防效果。
给饮用含1.5%（w/v）牛磺酸或1.5%（w/v）甜菜碱的水预处理4周的大鼠腹腔注射脂多糖（10mg/kg），并测定血浆转氨酶活性以及肝脏丙二醛、二烯共轭物（DC）、谷胱甘肽、α-生育酚和抗坏血酸水平，以及超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶活性。
脂多糖处理6小时后，观察到血浆转氨酶活性、肝脏丙二醛和DC水平显著升高，肝脏谷胱甘肽和α-生育酚水平以及SOD和谷胱甘肽过氧化物酶活性降低。与对照组相比，该处理未改变肝脏中的抗坏血酸水平。在注射脂多糖的大鼠中，牛磺酸或甜菜碱预处理导致血浆转氨酶活性、肝脏丙二醛和DC水平显著降低，谷胱甘肽和α-生育酚（甜菜碱无此作用）水平显著升高，而肝脏中的抗坏血酸水平以及SOD和谷胱甘肽过氧化物酶活性未改变。
我们的研究结果清楚地表明，牛磺酸或甜菜碱预处理对预防脂多糖诱导的肝毒性和促氧化状态有效。
