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目的 研究和比较增生性瘢痕和瘢痕疙瘩成纤维细胞经Fas单抗（FasMcab）诱导产生凋亡的能力，同时探讨Ca2+在其相应死亡信号通道中的作用。方法 取手术切除的增生性瘢痕和瘢痕疙瘩组织各6例，通过细胞培养6~8代后，以FasMcab为处理因素作用于增生性瘢痕及瘢痕疙瘩成纤维细胞24 h。应用透射电镜证实凋亡现象的发生，流式细胞仪检测并比较两者凋亡率。同时，应用粘附式细胞仪检测FasMcab作用下胞内Ca2+的变化。结果 增生性瘢痕成纤维细胞在工作浓度以上的FasMcab作用下，发生明显的凋亡现象，其凋亡率随着单抗浓度的增高不断增高。瘢痕疙瘩成纤维细胞在各浓度梯度下，均未发生明显凋亡，且各组间差异无显著意义。在FasMcab作用下，增生性瘢痕成纤维细胞内Ca2+显著增高而瘢痕疙瘩成纤维细胞内Ca2+无变化。结论 Fas介导凋亡的异常可能是瘢痕疙瘩成纤维细胞增殖-凋亡调控异常的细胞生物学机制之一，胞内Ca2+产生的障碍可能与其Fas介导凋亡的异常密切相关。
Objective To investigate the ability of fibroblasts and hypertrophic scars and keloid fibroblasts to induce apoptosis induced by Fas monoclonal antibody (FasMcab), and to explore the role of Ca2 + in their corresponding death signaling pathways. Methods Hypertrophic scars and keloid tissues were excised from 6 cases each. After cultured for 6 to 8 passages, FasMcab was used as a treatment factor in hypertrophic scars and keloid fibroblasts for 24 hours. Transmission electron microscopy was used to confirm the occurrence of apoptosis. Flow cytometry was used to detect and compare the apoptosis rates. At the same time, the change of intracellular Ca2 + with FasMcab was detected by Adherent Cytometry. Results Hypertrophic scar fibroblasts developed obvious apoptosis under the action concentration of FasMcab. The apoptosis rate increased with the increase of the concentration of McAb. There was no significant apoptosis of keloid fibroblasts in all concentration gradients, and there was no significant difference among the groups. Under the action of FasMcab, Ca2 + in hypertrophic scar fibroblasts was significantly increased while there was no change in Ca2 + in keloid fibroblasts. Conclusion Fas - mediated apoptosis may be one of the cellular mechanisms of keloid fibroblast proliferation - apoptosis regulation. The disorder of intracellular Ca2 + may be closely related to the abnormality of Fas - mediated apoptosis.