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目的探讨尼古丁对大鼠胸主动脉血管平滑肌细胞(VSMCs)的细胞外基质(ECM)表达的影响及可能的机制。方法用终浓度为100μmol/L的尼古丁作用于体外培养的大鼠VSMCs 24 h,以不加尼古丁的细胞为对照组,采用反转录-聚合酶链式反应(RT-PCR)、免疫印迹(Western blotting)方法检测ECM包括Ⅰ型胶原、纤维黏连蛋白和膜受体整合素表达的差异,以及可能参与信号转导的蛋白激酶p38的活性变化。结果与对照组相比,尼古丁刺激组细胞的两种细胞外基质包括I型胶原和纤维黏连蛋白及膜受体整合素β1的表达均升高,分别为对照组的1.8倍、1.7倍和1.6倍,差异显著(P<0.05);尼古丁刺激组的蛋白激酶p38的活性比对照组高1.95倍,差异极其显著(P<0.01);p38的活性被特异抑制剂SB202190抑制后,尼古丁诱导的I型胶原的表达也随之下降。结论 p38参与尼古丁诱导的细胞外基质的高表达。
Objective To investigate the effect of nicotine on the extracellular matrix (ECM) expression in rat thoracic aorta vascular smooth muscle cells (VSMCs) and its possible mechanism. Methods The VSMCs cultured in vitro were treated with nicotine at a final concentration of 100 μmol / L for 24 h. The cells without nicotine were used as control. Reverse transcription-polymerase chain reaction (RT-PCR), Western blotting Western blotting was used to detect the expression of ECM including type Ⅰ collagen, fibronectin and membrane receptor integrin, and the changes of p38 activity that may be involved in signal transduction. Results Compared with the control group, the expressions of two types of extracellular matrix including type I collagen, fibronectin and integrin β1 in the nicotine stimulated group were significantly increased, which were 1.8 times and 1.7 times and (P <0.05). The activity of p38 in nicotine-stimulated group was 1.95 times higher than that in control group (P <0.01), and the activity of p38 was inhibited by nicotine-specific inhibitor SB202190 Type I collagen expression also decreases. Conclusions p38 is involved in nicotine-induced high expression of extracellular matrix.