Effect of piroxicam on matrix metalloproteinase 2 and apoptosis.

A Mirshafiey, F Vaezzadeh, M R Khorramizadeh, F Saadat
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Abstract

We examined the effect of a nonsteroidal anti-inflammatory drug (NSAID), piroxicam, on apoptosis and matrix metalloproteinase 2 (MMP-2) activity compared with diclofenac and dexamethasone. The fibrosarcoma (WEHI-164) cell line was used to assess tolerability, MMP-2 activity and apoptosis. Piroxicam, dexamethasone and diclofenac were used at concentrations of 10-200 microg/ml in triplicate and 2-fold dilutions. MMP-2 activity was assessed using zymography. For assessment of apoptosis, the terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) method was used. The results of this study show that piroxicam is able to diminish MMP-2 activity and induce apoptosis under in vitro conditions. Piroxicam also showed high tolerability compared with diclofenac and dexamethasone. In conclusion, piroxicam is able to induce apoptosis and suppress MMP-2 activity.

吡罗昔康对基质金属蛋白酶2及细胞凋亡的影响。
与双氯芬酸和地塞米松相比,我们研究了非甾体抗炎药吡罗西康对细胞凋亡和基质金属蛋白酶2 (MMP-2)活性的影响。采用纤维肉瘤(WEHI-164)细胞系评估耐受性、MMP-2活性和凋亡。吡罗昔康、地塞米松和双氯芬酸的浓度为10-200微克/毫升,稀释倍数为3倍和2倍。利用酶谱法评估MMP-2活性。采用末端脱氧核糖核苷酸转移酶介导的dUTP镍端标记(TUNEL)方法评估细胞凋亡。本研究结果表明,在体外条件下,吡罗昔康能够降低MMP-2活性并诱导细胞凋亡。与双氯芬酸和地塞米松相比,吡洛昔康也表现出较高的耐受性。由此可见,吡罗昔康具有诱导细胞凋亡和抑制MMP-2活性的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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