β_1转化生长因子刺激兔耳皮肤瘢痕增生中蛋白酪氨酸激酶活性的变化

Effects of TGF-β_1 on activity of protein tyrosine kinase in scar tissue of rabbit ear

目的 观察 β1转化生长因子 (transforminggrowthfactorβ1,TGF β1)对兔耳皮肤瘢痕组织酪氨酸激酶 (proteintyrosinekinase,PTK)活性的影响 ,探讨受体PTK在TGF β1刺激瘢痕增生中的信号作用。方法 在兔耳腹侧伤口外用或瘢痕内注射TGF β1(5 μg/L) ,观察瘢痕变化。用3 2 P掺入法测定伤口伤前皮肤、上皮化及其后 14、30、4 5、6 0d非增生性瘢痕组织的PTK活性。结果 增生性瘢痕组织的PTK活性 [(4.4 0± 1.31)～ (4.91± 1.32 ) pmol·min-1·mg-1]高于正常皮肤组织 [(2 .87± 0 .96 ) pmol.min-1·mg-1](P <0 .0 0 1或 0 .0 1) ,而非增生性瘢痕仅在上皮化时 [(2 .81± 0 .87) pmol·min-1·mg-1]高于伤前 [(4.35± 1.2 6 )pmol·min-1·mg-1](P <0 .0 1) ,上皮化后 ,增生性瘢痕的PTK活性均高于非增生性瘢痕 (P <0 .0 0 1或 0 .0 1)。上皮化前后使用TGF β1不改变PTK活性 (P >0 .0 5 ) ,但显著刺激瘢痕增生 (P <0 .0 5或 0 .0 1)。结论 TGF β1没有改变PTK活性 ,提示TGF β1不经活化PTK刺激瘢痕增生。

Objective To observe the changes of protein tyrosine kinase (PTK) activity in scar tissue of rabbit ear induced by TGF-β_1 and to investigate the signal mechanism of TGF-β_1 in the scar proliferation. Methods TGF-β_1 (5 ng/ml) was applied on the wound and in the scar of rabbit ear. The PTK activity in the tissues from normal control, and 0, 14, 30, 45, and 60 d after wound epithelization was measured by phosphorus ( 32 P) incoporation. The scar changes were also observed. Results PTK activity in hypertrophic scar tissue [from (4.40±1.31) to (4.91±1.32)pmol·min -1 ·mg -1 ] was obviously elevated as compared with(2.87±0.96) pmol·min -1 mg -1 of normal skin ( P <0.001 or 0.01). PTK activity in normal scar tissue after wound epithelization had recovered to the basic level ( P >0.05). Furthermore, PTK activity of hypertrophic scar tissue was obviously elevated as compared with that of normal scar tissue ( P <0.001 or 0.01) Using TGF-β_1 before or after wound epithelization did not change PTK activity of all tissues ( P >0.05) but could accelerate scar hypertrophy ( P <0.005 or 0.01). Conclusion The unchangeable PTK activity of all the scar tissue by TGF-β_1 suggests that PTK may not mediate the signal of TGF-β_1 to accelerate scar hypertrophy.