益肝康抑制肝星状细胞Ⅰ型胶原合成的作用机制  

Inhibition of Yigankang on type Ⅰ collagen synthesis in rat HSCs induced by interleukin-1β

作　　者：姚希贤[1] 张亚平[2] 赵霞[3] 

机构地区：[1]河北医科大学第二医院消化内科,河北石家庄050000 [2]河北医科大学第三医院儿科 [3]首都医科大学宣武医院医院管理感染科

出　　处：《中西医结合肝病杂志》2007年第3期159-161,共3页Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases

摘　　要：目的:探讨活血化瘀中药复方“益肝康”抑制肝星状细胞Ⅰ型胶原合成的作用机制。方法:应用West-ern印记检测p38的活化程度;3H-Pro掺入法检测Ⅰ型胶原合成。结果:IL-1β有明显促大鼠HSCⅠ型胶原合成作用,IL-1β(10μg/L)作用培养的HSC24小时后,3H-Pro掺入量明显高于对照组(618.33±52.69vs388.83±49.72,P<0.01),阻断p38通路后,IL-1β的促HSCⅠ型胶原合成作用受到抑制。经不同浓度p38特异性阻断剂SB203580(10μmol/L,20μmol/L,40μmol/L)预处理的各组细胞,3H-Pro掺入量分别为487.33±42.75、408.50±27.47、400.83±19.49,与对照组(未用SB203580预处理,629.67±69.88)相比,其掺入量均明显降低(P<0.01,P<0.01,P<0.01)。益肝康可抑制IL-1β诱导的HSC中p38活性,与未用IL-1β处理组相比,在分别刺激HSCs5分钟、15分钟、30分钟和60分钟,HSC p38活性受到明显抑制(P<0.05,P<0.01)。经益肝康浸膏预孵育的益肝康+IL-1β组与单纯IL-1β组相比,p38活性明显受到抑制(1.550±0.410vs2.973±0.953,P<0.01)。结论:IL-1β可促进大鼠HSCⅠ型胶原合成;细胞内p38信号蛋白参与了IL-1β促HSCⅠ型胶原合成;益肝康可通过阻断p38通路,从而发挥抑制HSCⅠ型胶原合成作用。Objective： To study the mechanism of Yigankang inhibiting typeⅠ collagen synthesis in rat HSCs induced by interleukin-1β. Methods： Activation of p38 was detected with Western blotting, while the typeⅠ collagen synthesis in rat HSCs was examined by ^3H-Pro incorporation. Results： Interleukin-1β could intimulate typeⅠ collagen synthesis in rat HSCs, and HSCs typeⅠ collagen synthesis increased obviously after stimulation with IL-1β for 24h （618.33 ± 52. 69 vs 388.83 ± 49. 72, P 〈 0. 01 ）. Type Ⅰ collagen synthesis induced by IL-1β trended decrease in 3 groups pretreated with different concentrations of p38 inhibitor SB2035800 （ 10μmol/L, 487.33 ± 42. 75 ; 20μmol/L, 408. 50 ± 27.47 ; 40μmol/L, 400. 83 ± 19.49）. In comparison with control group （629. 67 ± 69. 88）, their decreases were all significant （P 〈0. 01, P 〈0. 01, P 〈 0. 01 ） ; IL-1β activated p38 in a time-dependent manner in rat HSCs. In comparison with group （without IL-1β treatment） , there exist significant difference at 5 min （ P 〈 0. 05 ）, 15 min （ P 〈 0. 01 ）, 30 min （ P 〈 0. 01 ） and 60 min （ P 〈 0. 01 ）. Yigankang could obviously inhibit activity of p38 induced by IL-1β （ 1. 550 ± 0. 410 vs 2. 973 ± 0. 953, P 〈 0. 01 ）. Conclusion： Intedeukin-1β could stimulate typeⅠ collagen synthesis in rat HSCs, and p38 signal pathway was involved in the process by IL-1β. Yigankang could inhibit HSCs typeⅠ collagen synthesis induced by IL-1β through p38 pathway.

关 键 词：益肝康/药效学 P38 白细胞介素-1Β 肝星状细胞 Ⅰ型胶原合成 大鼠 

分 类 号：R285[医药卫生—中药学]