Nikbakht Mohammad Reza, Ashrafi-Kooshk Mohammad Reza, Jaafari Morteza, Ghasemi Moosa, Khodarahmi Reza
Faculty of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Iran J Pharm Res. 2014 Spring;13(2):599-612.
Timolol is a non-selective beta-adrenergic receptor antagonist administered for treating glaucoma, heart attacks and hypertension. In the present study, we set out to determine whether or not timolol can provoke cataract formation, thus the influence of timolol on the amyloid-type aggregation of crystallin was investigated. We then provided experimental evidence of crystallin aggregation and its induction by timolol using different spectroscopic measurements. Turbidimetric measurements as well as ThT fluorescence data indicated that timolol induce extent of crystallin amyloid formation. The kinetic of protein aggregation was also changed in presence of increasing concentrations of the drug suggesting that long-term drug administration may contribute to the development of cataract. Since the consequence of timolol-crystallin interaction has yet to be identified, additional data on it may help us to postpone amyloid cataract formation.
噻吗洛尔是一种非选择性β-肾上腺素能受体拮抗剂，用于治疗青光眼、心脏病发作和高血压。在本研究中，我们着手确定噻吗洛尔是否会引发白内障形成，因此研究了噻吗洛尔对晶状体蛋白淀粉样聚集的影响。然后，我们使用不同的光谱测量方法提供了晶状体蛋白聚集及其由噻吗洛尔诱导的实验证据。比浊法测量以及硫代黄素T荧光数据表明，噻吗洛尔诱导了晶状体蛋白淀粉样形成的程度。在药物浓度增加的情况下，蛋白质聚集的动力学也发生了变化，这表明长期给药可能会导致白内障的发展。由于噻吗洛尔与晶状体蛋白相互作用的后果尚未确定，关于它的更多数据可能有助于我们延缓淀粉样白内障的形成。
