一种治疗钙通道阻滞剂引起的牙龈过度生长的可能方法

Q4 Pharmacology, Toxicology and Pharmaceutics

Oral Therapeutics and Pharmacology Pub Date : 2008-08-01 DOI:10.11263/JSOTP1982.27.103

H. Matsumoto, R. Takeuchi, M. Ono, Y. Akimoto, A. Fujii

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引用次数: 0

摘要

本研究总结硝苯地平应答者(NIFr)和硝苯地平无应答者(NIFn)的特征，并探讨了使用tenidap和18f¿-甘草次酸(18f¿-GA)治疗钙通道阻滞剂引起的牙龈过度生长的可能性。18f¿-GA抑制NIFr细胞增殖，诱导G1/S转变。在NIFr细胞中，细胞周期控制蛋白是18f¿-GA生长抑制活性的下游靶点。Tenidap释放细胞内Ca2+储存，导致NIFr细胞内Ca2+储存的消耗。它还抑制细胞生长，DNA和胶原合成，降低细胞内pH值，并增强NIFr细胞中基质金属蛋白酶-1的形成。上述结果提示，18f¿-GA和tenidap可有效预防钙通道阻滞剂引起的牙龈过度生长。

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A possible therapeutic for gingival overgrowth caused by calcium channel blockers

In the present study, the results of characters in nifedipine responders (NIFr) and nifedipine non-responders (NIFn) are summarized, and the possibility of using tenidap and 18ƒ¿ -glycyrrhetinic acid (18ƒ¿-GA) as a therapeutic for gingival overgrowth caused by calcium channel blockers is investigated. 18ƒ¿-GA inhibited cell proliferation and G1/S transition were induced in NIFr cells. It was also shown that cell cycle control proteins were down-stream targets in the growth-inhibition activity of 18ƒ¿-GA in NIFr cells. Tenidap discharges intracellular Ca2+ store, resulting in a depletion of intracellular Ca2+ store in NIFr cells. It also inhibits cell growth, DNA and collagen syntheses, lowered intracellular pH, and enhanced matrix metalloproteinase-1 formation in NIFr cells. These results suggest that 18ƒ¿-GA and tenidap might be effective for the prevention of gingival overgrowth caused by calcium channel blockers.

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来源期刊

Oral Therapeutics and Pharmacology Medicine-Pharmacology (medical)

CiteScore

0.10

自引率

0.00%

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