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研究观察了重组人白介素 10 (rhIL 10 )对晚期糖基化终产物 (AGE)刺激下离体大鼠胸主动脉血管平滑肌细胞增殖及对SD大鼠血管损伤后新生内膜增殖的影响。体外培养大鼠主动脉血管平滑肌细胞 ,采用MTS/PES法确定血管平滑肌细胞的增殖状态 ;应用流式细胞术测定细胞周期 ;利用 p44 / 42磷酸化抗MAPK抗体的蛋白免疫印迹法测定 p44 / 42MAPK磷酸化蛋白表达。利用大鼠颈动脉血管损伤模型 ,观察rhIL 10对新生内膜增殖的影响。结果显示 :( 1)AGE处理组与对照组相比 ,AGE对血管平滑肌细胞增殖具有明显的刺激作用 (P <0 0 5 )。rhIL 10单独应用对血管平滑肌细胞生长没有影响 (P >0 0 5 )。在AGE刺激下 ,低至 10 0ng/ml的rhIL 10可抑制血管平滑肌细胞的生长 (P <0 0 5 )。( 2 )流式细胞术测定的结果显示 ,rhIL 10可以使AGE作用下的VSMC大部分处于G0 /G1期 ,与对照组相比有明显差异 (P <0 0 1)。 ( 3 )AGE对 p44 / p42MAPK磷酸化蛋白表达有显著的增强作用 ,此作用可被rhIL 10抑制 (P <0 0 0 1)。( 4)大鼠颈动脉损伤后 ,rhIL 10治疗组的动脉血管新生内膜 /中层面积比低于对照组约45 % (P <0 0 1)。表明抗炎细胞因子rhIL 10可抑制AGE诱导的大鼠血管平滑肌细胞增殖和血管新生内膜的增殖
The effects of recombinant human interleukin 10 (rhIL 10) on the proliferation of thoracic aorta vascular smooth muscle cells (VSMCs) stimulated by advanced glycation end products (AGE) and the proliferation of neointima in SD rats after vascular injury were observed. The aortic vascular smooth muscle cells were cultured in vitro and the proliferation status of vascular smooth muscle cells was determined by MTS / PES method. The cell cycle was determined by flow cytometry. The p44 / 42 MAPK protein was detected by Western blotting using p44 / 42 phosphorylated anti-MAPK antibody Phosphorylated protein expression. The rat model of carotid artery vascular injury was used to observe the effect of rhIL 10 on neointimal hyperplasia. The results showed that: (1) Compared with the control group, AGE significantly stimulated the proliferation of vascular smooth muscle cells (P <0.05). rhIL 10 alone had no effect on vascular smooth muscle cell growth (P> 0.05). Under AGE stimulation, rhIL 10 down to 10 ng / ml inhibited the growth of vascular smooth muscle cells (P <0 05). (2) The results of flow cytometry showed that most of VSMCs under the action of AGE were in G0 / G1 phase, which was significantly different from the control group (P <0.01). (3) AGE significantly enhanced p44 / p42MAPK phosphorylation protein expression, which was inhibited by rhIL 10 (P <0.01). (4) The ratio of neointima / medial area of arteries in rhIL 10-treated group was lower than that in control group by 45% (P <0.01) after carotid artery injury in rats. Anti-inflammatory cytokine rhIL 10 could inhibit the AGE-induced rat vascular smooth muscle cell proliferation and angiogenesis intimal proliferation