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目的探讨黄芩素对人体瘢痕疙瘩成纤维细胞在增殖、凋亡的影响,为临床瘢痕疙瘩的治疗提供实验基础。方法 MTT法测定黄芩素干预后瘢痕疙瘩成纤维细胞的活力和乳酸脱氢酶的含量;Annexin V-FITC分析成纤维细胞在干预后的细胞凋亡率;蛋白印迹实验检测凋亡蛋白表达水平的变化。结果黄芩素对体外培养的瘢痕疙瘩成纤维细胞的增殖有抑制作用(P<0.01),抑制效应呈剂量依赖性,作用24 h后,黄芩素50μM组抑制率为65%,IC50值为(31.34±0.29)μM;黄芩素还可诱导瘢痕疙瘩成纤维细胞凋亡,黄芩素25μM组凋亡率达22.7%,和对照组相比,差异有统计学意义(P<0.01);但不影响乳酸脱氢酶的含量。黄芩素作用后明显降低线粒体膜电位,上调凋亡蛋白裂解半胱天冬酶3和裂解半胱天冬酶9的表达,裂解半胱天冬酶8的表达不受影响。结论黄芩素通过抑制细胞增殖和促进细胞凋亡来抑制瘢痕疙瘩生长。
Objective To investigate the effects of baicalein on the proliferation and apoptosis of human keloid fibroblasts and to provide experimental basis for the treatment of clinical keloid. Methods The activity of keloid fibroblasts and the content of lactate dehydrogenase in keloid fibroblasts were detected by MTT assay. The apoptosis rate of fibroblasts after intervention was analyzed by Annexin V-FITC. The protein expression of apoptosis was detected by Western blotting Variety. Results Baicalein inhibited the proliferation of cultured keloid fibroblasts in vitro (P <0.01), and the inhibitory effect was dose-dependent. After 24 h treatment, baicalein inhibited the proliferation of keloid fibroblasts by 65% and the IC50 values were (31.34 ± 0.29) μM. Baicalein could also induce the apoptosis of keloid fibroblasts. The apoptosis rate of keloid fibroblasts in baicalein group was 22.7%, which was significantly different from the control group (P <0.01) Dehydrogenase content. Baicalein significantly decreased the mitochondrial membrane potential, up-regulated the expression of caspase-3 and caspase-9, and cleaved Caspase-8 expression was not affected. Conclusion Baicalein can inhibit the growth of keloid by inhibiting cell proliferation and promoting cell apoptosis.