Inhibition of α_1(Ⅰ) collagen gene in vitro transcription by antisense oligodeoxynucleotides

Objective and Methods: Excessive accumulation of collagen typeⅠ and type Ⅲ causes the formation of keloids and hypertrophic scars. To understand the mechanism by which antisense oligodeoxynucleotide (Oligo) acts on in vitro transcrption α1 (I) collagen gene, isotopes (α-32pGTP) was incorporated into 2 SP6 in vitro transcription systems. Results and Conclu- sion: Oligo 2 (at the transcription start region) could effectively inhibit in vitro transcription of pGEM3-Col13 and the control (random oligodeoxynucleotides) showed no inhibition. However, oligo 1 (at the transcription start region) obviously inhibited the in vitro transcription of pGEM3-Col14, while Oligo 2, which targeted at the down stream region (about 200 bp) of the promoter showed no significant inhibition effect.

血小板源性伤口愈合因子促糖尿病大鼠伤口愈合与成纤维细胞前胶原Ⅰ型(α_1)基因表达的关系

目的研究外源性血小板源性伤口愈合因子（ＰＤＷＨＦ）对糖尿病大鼠伤口愈合的作用及其机理。方法通过糖尿病大鼠背部成对切口伤模型证实ＰＤＷＨＦ应用于伤口局部的情况。结果伤后７、１０及１４天，糖尿病治疗组及糖尿病自身对照组伤口抗张力值分别为１００．９４±１２．７４、２４４．０２±４８．０２、５３５．０８±３６．２６和６５．６６±１１．７６、１１０．７４±２７．４４、２７１．４６±２９．８０Ｎ／ｍ，两组间差异显著（Ｐ＜０．０１）。体外实验发现，生长融合的伤口成纤维细胞与ＰＤＷＨＦ孵育４、８及１２小时后，ＰＤＷＨＧ组前胶原Ⅰ型（α１）ｍＲＮＡ分别较对照组高０．９、３．７及２．２倍。

低氧对人胚肺成纤维细胞增殖及I型前胶原基因表达的影响

目的阐明低氧在血管壁构形重组中的作用及川芎嗪的疗效机理。方法用细咆计数法及非放射性细胞增殖检测法观察2%低氧对人胚肺成纤维细胞增殖的影响;用Northern印迹杂交法检测2%低氧对人胚肺成纤维细胞Ⅰ型前胶原基因表达的作用及川芎嗪对基因表达的影响。结果低氧24.48及72h能明显促进人胚肺成纤维细胞增殖;低氧24h Ⅰ型前胶原基因表达明显升高;川芎嗪(30μg/ml及10μg/ml)可抑制上述基因表达的升高。结论低氧对人胚肺成纤维细胞有直接利激作用,通过促进其增殖及前胶原基因表达而影响肺血管构形重组和损伤组织的修复。