Lee Myeong Soo, Kim Myung-Sunny, Park Soo Young, Kang Chang-Won
Complementary Medicine, Peninsula Medical School, Universities of Exeter and Plymouth, Exeter EX2 4NT, United Kingdom.
World J Gastroenterol. 2006 Mar 21;12(11):1718-22. doi: 10.3748/wjg.v12.i11.1718.
To evaluate the effects of betaine on the ethanol-induced secretion of IGF-I and IGFBP-1 using radioimmunoassay and Western blotting, respectively, in primary cultured rat hepatocytes.
Hepatocytes isolated from male Sprague-Dawley rats were incubated with various concentrations of ethanol and PD98059 procedures. The hepatocytes were also treated with different doses of betaine (10(-5), 10(-4), and 10(-3) mol/L). We measured IGF-I and IGFBP-1 using radioimmunoassay and Western blotting, respectively.
The ethanol-induced inhibition of IGF-I secretion was attenuated by betaine in a concentration-dependent manner in primary cultured rat hepatocytes. At 10(-3) mol/L, betaine significantly increased IGF-I secretion but decreased IGFBP-1 secretion. In addition, p42/44 mitogen-activated protein kinase (MAPK) activity was accelerated significantly from 10 min to 5 h after treatment with 10(-3) mol/L betaine. Furthermore, the changes in IGF-1 and IGFBP-1 secretion resulting from the increased betaine-induced p42/44 MAPK activity in primary cultured rat hepatocytes was blocked by treatment with the MAPK inhibitor PD98059. Betaine treatment blocked the ethanol-induced inhibition of IGF-I secretion and p42/44 MAPK activity, and the ethanol-induced increase in IGFBP-1 secretion.
Betaine modulates the secretion of IGF-I and IGFBP-1 via the activation of p42/44 MAPK in primary cultured rat hepatocytes. Betaine also alters the MAPK activations induced by ethanol.
分别采用放射免疫分析法和蛋白质免疫印迹法,评估甜菜碱对原代培养大鼠肝细胞中乙醇诱导的胰岛素样生长因子-I(IGF-I)和胰岛素样生长因子结合蛋白-1(IGFBP-1)分泌的影响。
将从雄性Sprague-Dawley大鼠分离的肝细胞与不同浓度的乙醇及PD98059进行孵育。肝细胞还分别用不同剂量的甜菜碱(10⁻⁵、10⁻⁴和10⁻³mol/L)处理。我们分别采用放射免疫分析法和蛋白质免疫印迹法检测IGF-I和IGFBP-1。
在原代培养的大鼠肝细胞中,甜菜碱以浓度依赖的方式减弱了乙醇诱导的IGF-I分泌抑制作用。在10⁻³mol/L时,甜菜碱显著增加IGF-I分泌,但降低IGFBP-1分泌。此外,在用10⁻³mol/L甜菜碱处理后10分钟至5小时,p42/44丝裂原活化蛋白激酶(MAPK)活性显著加快。此外,原代培养大鼠肝细胞中甜菜碱诱导的p42/44 MAPK活性增加所导致的IGF-1和IGFBP-1分泌变化,被MAPK抑制剂PD98059处理所阻断。甜菜碱处理阻断了乙醇诱导的IGF-I分泌抑制和p42/44 MAPK活性,以及乙醇诱导的IGFBP-1分泌增加。
在原代培养的大鼠肝细胞中,甜菜碱通过激活p42/44 MAPK调节IGF-I和IGFBP-1的分泌。甜菜碱还改变了乙醇诱导的MAPK激活。