![]() |
![]() |
|
总体应用的维生素C增强人类真皮中胶原质I和III、其加工酶和组织间质金属蛋白酶抑制剂的mRNA水平 Ascorbic acid (vitamin C) is a cofactor
required for the function of several hydroxylases and monooxygenases.
It is not synthesized in humans and some other animal species and has
to be provided by diet or pharmacologic means. Its absence is responsible
for scurvy, a condition related in its initial phases to a defective synthesis
of collagen by the reduced function of prolylhydroxylase and production
of collagen polypeptides lacking hydroxyproline, therefore, they are unable
to assemble into stable triple-helical collagen molecules. In fibroblast
cultures, vitamin C also stimulates collagen production by increasing
the steady-state level of mRNA of collagen types I and III through enhanced
transcription and prolonged half-life of the transcripts. The aim of the
experimental work has been to evaluate the effect on dermal cells of a
preparation of vitamin C topically applied on one side vs placebo on the
other side of the dorsal face of the upper forearm of postmenopausal women.
Biopsies were collected on both sides and the level of mRNA measured by
non competitive reverse transcription-polymerase chain reaction made quantitative
by the simultaneous transcription and amplification of synthetic RNA used
as internal standards. The mRNA of collagen type I and type III were increased
to a similar extent by vitamin C and that of three post-translational
enzymes, the carboxy- and amino-procollagen proteinases and lysyloxidase
similarly increased. The mRNA of decorin was also stimulated, but elastin,
and fibrillin 1 and 2 were not modified by the vitamin. The expression
of matrix metalloproteinases 1, 2, and 9 was not significantly changed,
but an increased level of tissue inhibitor of matrix metalloproteinase
1 mRNA was observed without modification of tissue inhibitor of matrix
metalloproteinase 2 mRNA. The stimulating activity of topical vitamin
C was most conspicuous in the women with the lowest dietary intake of
the vitamin and unrelated to the level of actinic damage. The results
indicate that the functional activity of the dermal cells is not maximal
in postmenopausal women and can be increased. [引自J Invest Dermatol 2001 Jun;116(6):853-859] |