[1]吴江群,聂兴举,秦泽莲.氧化苦参碱对病理性瘢痕成纤维细胞增殖凋亡的影响[J].中国微创外科杂志,2011,11(3):259-263.
　Wu Jiangqun,Nie Xingjiu,Qin Zelian..Effect of Oxymatrine on Cell Proliferation, Apoptosis, Cell Cycle and ERK1 Expression of the Fibroblasts Derived from Hypertrophic Scar and Keloids[J].Chinese Journal of Minimally Invasive Surgery,2011,11(3):259-263.
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氧化苦参碱对病理性瘢痕成纤维细胞增殖凋亡的影响 ()
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《中国微创外科杂志》[ISSN:1009-6604/CN:11-4526/R]

卷:
11
期数:
2011年3期
页码:
259-263
栏目:
基础研究
出版日期:
2011-03-20

文章信息/Info

Title:
Effect of Oxymatrine on Cell Proliferation, Apoptosis, Cell Cycle and ERK1 Expression of the Fibroblasts Derived from Hypertrophic Scar and Keloids
作者:
吴江群; 聂兴举; 秦泽莲
北京大学第三医院成形外科，北京100191
Author(s):
Wu Jiangqun;  Nie Xingjiu; Qin Zelian.
Department of Plastic Surgery, Peking University Third Hospital, Beijing 100191, China
关键词:
氧化苦参碱; 氢化可的松; 成纤维细胞; 增殖; 凋亡
Keywords:
Oxymatrine; Hydrocortisone; Fibroblast; Proliferation; Apoptosis
分类号:
R34
文献标志码:
A
摘要:
目的观察氧化苦参碱（oxymatrine，OM）对人病理性瘢痕成纤维细胞增殖、凋亡、细胞周期及细胞外信号调节激酶1（ERK1）的影响，并且与瘢痕治疗常规药物氢化可的松（hydrocortisone，HC）的作用进行比较。方法原代的瘢痕疙瘩、增生性瘢痕和正常皮肤的成纤维细胞（KFb、HFb、NFb）采用组织块培养法培养，将氧化苦参碱（2×10-6 mol/L）、氢化可的松（5.5×10-9 mol/L）分别作用于KFb、HFb、NFb，用四甲基偶氮唑蓝微量酶反应比色法（MTT）检测细胞增殖活力，流式细胞仪检测细胞凋亡、细胞周期、ERK1的变化。结果OM能明显抑制KFb、HFb和NFb的增殖活性（抑制率分别为12%，14%，10%），促进KFb的凋亡（增加72%）。HC明显抑制KFb、HFb、NFb的增殖（抑制率分别为21%，21%，15%），并促进其凋亡（分别增加184%、121%和148%）。上述改变均有统计学意义。OM、HC对三种细胞的细胞周期及ERK1表达无显著作用。结论类似氢化可的松，氧化苦参碱通过抑制瘢痕疙瘩、增生性瘢痕、正常皮肤成纤维细胞的增殖和促进瘢痕疙瘩成纤维细胞的凋亡作用而可能应用于瘢痕疙瘩和增生性瘢痕的治疗。
Abstract:
ObjectiveTo study the effects of oxymatrine (OM) and hydrocortisone (HC) on the function of the fibroblasts from keloid (KFb), hypertrophic scar (HFb), and normal skin (NFb). At mean time, to observe the differences in cell proliferation, apoptosis, cell cycle and the expression of ERK1 among KFb, HFb, and NFb. MethodsKFb, HFb and NFb were derived from patients and then cultured in vitro. MTT were used to examine cell proliferation. Flow cytometry and FITCAnnexin VPI doubled staining were employed to analyze cell apoptosis, cell cycle, and the expression of ERK1. ResultsOM decreased cell proliferation of KFb, HFb and NFb (inhibition rates were 12%, 14%, and 10%, respectively) but increased apoptosis by 72% in KFb. HC decreased cell proliferation of KFb, HFb and NFb (inhibition rates were 21%, 21% and 15%, respectively), but increased cell apoptosis of KFb, HFb and NFb by 184%, 121%, and 148%, respectively. Above data were significant in statistics. There were no any difference in cell cycle and ERK1 expression among the groups. ConclusionsSimilarly with HC, OM can control keloid and hypertrophic scar by suppressing fibroblast proliferation and inducing cell apoptosis.

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备注/Memo

备注/Memo:
国家自然科学基金资助课题（30170971）秦泽莲通讯作者，Email:qinzl@bjmu.edu.cn
更新日期/Last Update: 2013-04-18