IFN-γ抑制兔耳皮肤伤口愈合和瘢痕增生中蛋白激酶C的活性变化

Activity changes of protein kinase C in effect of interferon-γ on wound healing and cicatrisation

目的观察IFN-γ抑制兔耳伤口愈合和瘢痕形成中肉芽组织和瘢痕组织中蛋白激酶C（Protein Kinase C，PKC）活性的变化，探讨PKC的信号作用。方法兔耳伤口或瘢痕组织内使用IFN-γ，用^32P掺入底物法测定伤后3、6d、上皮化时（11～16d），上皮化后14、30和45d瘢痕组织的PKC活性，并观察上皮化时间和瘢痕变化。结果肉芽组织、周边组织和瘢痕组织的PKC活性伤后持续升高（P〈0．01），IFN-γ没有改变PKC活性（P〉0．05，）但延迟创面愈合约1．5d（P〈0．01），并抑制瘢痕增生（P〈0．05）。结论IFN-γ抑制伤口愈合和瘢痕增生的作用不经PKC介导；PKC活化与伤口愈合和瘢痕增生有关。

Objective To study the roles of protein kinase C （PKC） in effect of interferon-γ （IFN-γ） on wound healing and cicatrization. Methods IFN-γwas applied on the wound and into the scar tissues of rabbit ear before or after wound healing. PKC activities in the tissues from 0, 3, 6 d, 11-16 d post-wounding and from 14, 30 and 45d post-epithelization were measured by phosphorus （32 p） incoporation. The time of wound epithelization and scar changes were also observed. Results The PKC activity in granulation tissue, wound margin tissue and scar tissue elevated obviously in comparing with that of normal skin （P 〈 0.01 ）. IFN-γdid not change PKC activity （P 〉 0.05）. But it delayed the wound healing （P 〈 0.01 ） and inhibited scar hyperplasia （P 〈 0.05）. Conclusions PKC might not mediate the signal of IFN-γ inhibiting the wound healing and scar hyporplasia. But PKC might be related to the wound heahng and scar hyperplasia.