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首页> 外文期刊>World Journal of Gastroenterology >Effects of betaine on ethanol-stimulated secretion of IGF-I and IGFBP-1 in rat primary hepatocytes: involvement of p42/44 MAPK activation.
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Effects of betaine on ethanol-stimulated secretion of IGF-I and IGFBP-1 in rat primary hepatocytes: involvement of p42/44 MAPK activation.

机译：甜菜碱对大鼠原代肝细胞乙醇刺激的IGF-1和IGFBP-1分泌的影响：p42 / 44 MAPK激活的参与。

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AIM: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. METHODS: 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. RESULTS: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. CONCLUSION: 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.
机译：目的：分别用放射免疫法和蛋白质印迹法评估甜菜碱对乙醇诱导的IGF-I和IGFBP-1分泌的影响，其作用是原代培养的大鼠肝细胞。方法：将分离自雄性Sprague-Dawley大鼠的肝细胞与各种浓度的乙醇和PD98059程序一起孵育。还用不同剂量的甜菜碱处理肝细胞（10（-5），10（-4）和10（-3）mol / L）。我们分别使用放射免疫测定法和蛋白质印迹法测量了IGF-1和IGFBP-1。结果：甜菜碱以浓度依赖性的方式减弱了乙醇对原代培养大鼠肝细胞中IGF-I分泌的抑制作用。在10（-3）mol / L下，甜菜碱显着增加了IGF-1的分泌，但降低了IGFBP-1的分泌。此外，用10（-3）mol / L甜菜碱处理后，p42 / 44丝裂原激活的蛋白激酶（MAPK）活性从10分钟显着加速到5 h。此外，通过用MAPK抑制剂PD98059处理可阻止甜菜碱诱导的原代培养的大鼠肝细胞中由甜菜碱诱导的p42 / 44 MAPK活性增加而导致的IGF-1和IGFBP-1分泌变化。甜菜碱处理阻止了乙醇诱导的IGF-1分泌抑制和p42 / 44 MAPK活性，以及​​乙醇诱导的IGFBP-1分泌增加。结论：甜菜碱通过激活原代培养的大鼠肝细胞中的p42 / 44 MAPK来调节IGF-1和IGFBP-1的分泌。甜菜碱还可以改变乙醇诱导的MAPK活化。

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