Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.
Department of Cell Bank, Pasteur Institute of Iran, Tehran, Iran.
Iran Biomed J. 2020 Jul;24(4):243-50. doi: 10.29252/ibj.24.4.243. Epub 2020 Jan 22.
Our previous findings indicated that carvacrol and thymol alleviate cognitive impairments caused by Aβ in rodent models of Alzheimer's disease (AD). In this study, the neuroprotective effects of carvacrol and thymol against Aβ25-35-induced cytotoxicity were evaluated, and the potential mechanisms were determined.
PC12 cells were pretreated with Aβ25-35 for 2 h, followed by incubation with carvacrol or thymol for additional 48 h. Cell viability was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method. A flurospectrophotometer was employed to observe the intracellular reactive oxygen species (ROS) production. Protein kinase C (PKC) activity was analyzed using ELISA.
Our results indicated that carvacrol and thymol could significantly protect PC12 cells against Aβ25-35-induced cytotoxicity. Furthermore, Aβ25-35 could induce intracellular ROS production, while carvacrol and thymol could reverse this effect. Moreover, our findings showed that carvacrol and thymol elevate PKC activity similar to Bryostatin-1, as a PKC activator.
This study provided the evidence regarding the protective effects of carvacrol and thymol against Aβ25–35-induced cytotoxicity in PC12 cells. The results suggested that the neuroprotective effects of these compounds against Aβ25-35 might be through attenuating oxidative damage and increasing the activity of PKC as a memory-related protein. Thus, carvacrol and thymol were found to have therapeutic potential in preventing or modulating AD.
我们之前的研究结果表明，香芹酚和百里香酚可减轻阿尔茨海默病（AD）啮齿动物模型中 Aβ引起的认知障碍。在这项研究中，评估了香芹酚和百里香酚对 Aβ25-35 诱导的细胞毒性的神经保护作用，并确定了潜在的机制。
PC12 细胞用 Aβ25-35 预处理 2 h，然后用香芹酚或百里香酚孵育 48 h。用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐法测定细胞活力。使用荧光分光光度计观察细胞内活性氧（ROS）的产生。用 ELISA 法分析蛋白激酶 C（PKC）活性。
我们的结果表明，香芹酚和百里香酚可显著保护 PC12 细胞免受 Aβ25-35 诱导的细胞毒性。此外，Aβ25-35 可诱导细胞内 ROS 产生，而香芹酚和百里香酚可逆转此作用。此外，我们的研究结果表明，香芹酚和百里香酚可像 PKC 激活剂 Bryostatin-1 一样，提高 PKC 活性。
本研究为香芹酚和百里香酚对 PC12 细胞中 Aβ25-35 诱导的细胞毒性的保护作用提供了证据。结果表明，这些化合物对 Aβ25-35 的神经保护作用可能是通过减轻氧化损伤和增加与记忆相关的 PKC 活性来实现的。因此，香芹酚和百里香酚具有预防或调节 AD 的治疗潜力。
