Department of Biochemistry, University of Vermont, Burlington, VT, USA.
Wound Repair Regen. 1994 Oct;2(4):292-6. doi: 10.1046/j.1524-475X.1994.20410.x.
Inhibition of wound healing by anti-inflammatory steroids is associated with decreased collagen synthesis. Methyl-20-dihydroprednisolonate has been previously reported to be anti-inflammatory without inhibiting collagen synthesis in skin when given either subcutaneously or intraperitoneally. The data we now report show that this prednisolone derivative, as well as two 9alpha fluorinated derivatives inhibit both collagen synthesis and pro-alpha(1) (I) collagen gene promoter activity in rat skin fibroblasts. Our data suggest that metabolism, absorption, or distribution of these corticosteroids results in their inability to inhibit collagen synthesis in vivo. In addition our data indicate that fluorination in the 9alpha position of the adrenal steroid nucleus is not required for the inhibition of collagen synthesis by methyl-20-dihydroprednisolonate.
抗炎类固醇抑制伤口愈合与胶原合成减少有关。先前有报道称，当甲基-20-二氢泼尼松龙经皮下或腹腔给药时，具有抗炎作用而不抑制皮肤中的胶原合成。我们现在报告的数据表明，这种泼尼松龙衍生物以及两种 9α 位氟化衍生物可抑制大鼠皮肤成纤维细胞中的胶原合成和前α1(I)胶原基因启动子活性。我们的数据表明，这些皮质类固醇的代谢、吸收或分布导致其无法在体内抑制胶原合成。此外，我们的数据表明，肾上腺甾体核 9α 位的氟化对于甲基-20-二氢泼尼松龙抑制胶原合成不是必需的。
