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Molecular mechanisms of gallic acid-induced growth inhibition, apoptosis, and necrosis in hypertrophic scar fibroblasts

机译：高酸诱导的生长抑制，细胞凋亡和坏死在肥厚瘢痕成纤维细胞中的分子机制

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Abstract Aims To explore the effect and molecular mechanism of gallic acid (GA) on the cytostatic and cytotoxicity of hypertrophic scar fibroblasts (HSFs). Materials and methods HSFs were treated with a serial dose of GA for indicated time. The cytostatic and cytotoxicity of GA were evaluated by microscopy, trypan blue exclusion assay and LDH releasing. The mechanisms of GA-induced cytostatic were examined by cell cycle distribution assay and the expression of cell cycle-relative protein. GA-elicited apoptosis were verified by TUNEL assay, mitochondria membrane potential, caspase activity and the expression of apoptosis-relative protein. GA-induced necrosis was confirmed by lysosome rupture using acridine orange stain. Various blockers, including intracellular calcium chelator; BAPTA-AM, IP3R blocker; 2-APB, calpain inhibitor, ALLM and ALLN were used to address the signaling cascade in GA-induced HSF necrosis. Key findings GA-induced growth inhibition, apoptosis, and necrosis in HSFs depend on increasing dose. HSFs treated with GA at non-cytotoxic concentrations (50 to 75 μM) significant increased both the S- and G2/M-phase HSFs population, and this event was accompanied with down-regulation of cyclin A, cyclin B, CDK1 and CDK2. Incubation of HSFs with 100–150 μM of GA induced apoptosis through Bcl2/Bax-mitochondrial-dependent pathway. While the concentrations up to 200 μM of GA that elicited necrosis via a calcium/calpain I/lysosome rupture signaling axis. Interestingly, GA at 200 μM did not harm to keratinocyte. Significance These results revealed that GA might have the potential to be developed as a treatment for patients with hypertrophic scar.
机译：摘要旨在探讨小酸（GA）对肥厚瘢痕成纤维细胞（HSF）的细胞抑制和细胞毒性的影响和分子机制。材料和方法用序列剂量的GA处理HSF，用于指示时间。通过显微镜，台盼蓝排除测定和LDH释放评估Ga的细胞抑制和细胞毒性。通过细胞周期分布测定和细胞周期相对蛋白的表达检查了GA诱导的细胞抑制的机制。通过TUNEL测定，线粒体膜电位，胱天蛋白酶活性和凋亡相对蛋白表达验证GA引发的细胞凋亡。通过吖啶橙色染色的溶酶体破裂证实了GA诱导的坏死。各种阻滞剂，包括细胞内钙螯合剂; Bapta-am，IP3R阻止; 2-APB，CALPAIN抑制剂，ALLM和ALLN用于解决GA诱导的HSF坏死中的信号级联。关键发现GA诱导的生长抑制，细胞凋亡和HSF中的坏死取决于增加剂量。用非细胞毒性浓度（50至75μm）处理的HSF显着增加了S-和G2 / M相HSF群体，并且该事件伴随着细胞周期蛋白A，细胞周期蛋白B，CDK1和CDK2的调节。通过BCl2 / Bax-Mitocococalrial依赖性途径将HSF与100-150μm诱导细胞凋亡的孵育。虽然浓度高达200μm的GA通过钙/酸钙I /溶酶体破裂信号轴引发坏死。有趣的是，200μm的Ga对角蛋白细胞没有伤害。重要性这些结果表明，GA可能具有促进肥厚瘢痕患者的治疗潜力。

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