Karna Ewa, Trojan Sylwia, Pałka Jerzy A
Department of Medicinal Chemistry, Medical University in Białystok, 1 Kilińskiego St., 15-089 Białystok, Poland.
Acta Pol Pharm. 2009 May-Jun;66(3):229-33.
The data showing that butyrate may play an important role in cellular metabolism led us to study its effect on collagen biosynthesis in cultured fibroblasts. Since insulin-like growth factor-I (IGF-I) is the most potent stimulator of collagen biosynthesis in fibroblasts, the effect of butyrate on IGF-I receptor (IGF-IR) expression was evaluated. Confluent human dermal fibroblasts were treated with millimolar concentrations of sodium butyrate (NaB) for 48 hours. It was found that butyrate induced collagen biosynthesis and prolidase activity. It was found that the exposure of the cells to 4 mM butyrate contributed to a distinct increase in IGF-IR. It was accompanied by a parallel increase in the expression of Sos protein and MAP-kinases (ERK1, ERK2). It was found that the MEK inhibitor decreased collagen biosynthesis and expression of MAP-kinases (ERK1, ERK2), while NaB counteracted the process. The data suggests that butyrate-dependent stimulation of collagen biosynthesis in cultured human skin fibroblasts undergoes through IGF-IR signaling.
数据显示丁酸盐可能在细胞代谢中发挥重要作用，这促使我们研究其对培养的成纤维细胞中胶原蛋白生物合成的影响。由于胰岛素样生长因子-I（IGF-I）是成纤维细胞中胶原蛋白生物合成最有效的刺激因子，因此评估了丁酸盐对IGF-I受体（IGF-IR）表达的影响。将汇合的人皮肤成纤维细胞用毫摩尔浓度的丁酸钠（NaB）处理48小时。发现丁酸盐可诱导胶原蛋白生物合成和脯氨酰肽酶活性。发现将细胞暴露于4 mM丁酸盐会导致IGF-IR明显增加。同时Sos蛋白和MAP激酶（ERK1、ERK2）的表达也平行增加。发现MEK抑制剂可降低胶原蛋白生物合成和MAP激酶（ERK1、ERK2）的表达，而NaB可抵消这一过程。数据表明，丁酸盐依赖性刺激培养的人皮肤成纤维细胞中胶原蛋白生物合成是通过IGF-IR信号传导进行的。
