Departments of Physiology, School of Medicine, Sivas Cumhuriyet University, TR-58140, Sivas, Turkey.
Departments of Biochemistry, School of Pharmacy, Sivas Cumhuriyet University, Sivas, TR-58140, Turkey.
Metab Brain Dis. 2022 Apr;37(4):1221-1230. doi: 10.1007/s11011-022-00948-z. Epub 2022 Mar 14.
Recent studies have shown that angiotensin-converting enzyme (ACE) inhibitors have reduced oxidative damage in the central nervous system (CNS). Accumulating evidence have also demonstrated that captopril, an ACE inhibitor, has protective effects on the CNS. However, its effects on hydrogen peroxide (HO)-induced oxidative damage in glial cells and interaction with the inflammatory system are still uncertain. Therefore, this study was aimed to investigate the protective effect of captopril on glial cell damage after HO-induced oxidative stress involved in the inflammatory and apoptotic pathways. The control group was without any treatment, and the HO group was treated with 0.5 mM HO for 24 h. The captopril group was treated with various concentrations of captopril for 24 h. The captopril + HO group was pre-treated with captopril for 1 h and then exposed to 0.5 mM HO for 24 h. In the captopril + HO group, captopril at all concentrations significantly increased the cell viability in C6 cells. It also significantly increased the TAS and decreased the TOS levels which are an indicator of oxidative stress. Moreover, captopril significantly reduced the inflammation markers including NF-kB, IL-1 β, COX-1, and COX-2 levels. Flow cytometry results also exhibited that captopril pretreatment significantly decreased the apoptosis rate. Besides, captopril significantly reduced apoptotic Bax and raised anti-apoptotic Bcl-2 protein levels. In conclusion, captopril has protective effects on C6 cells after HO-induced oxidative damage by inhibiting oxidative stress, inflammation, and apoptosis. However, further studies need to be conducted to evaluate the potential of captopril as a neuroprotective agent.
最近的研究表明，血管紧张素转换酶（ACE）抑制剂可减少中枢神经系统（CNS）的氧化损伤。越来越多的证据表明，ACE 抑制剂卡托普利对中枢神经系统具有保护作用。然而，其对过氧化氢（HO）诱导的神经胶质细胞氧化损伤的作用及其与炎症系统的相互作用尚不确定。因此，本研究旨在探讨卡托普利在 HO 诱导的氧化应激涉及炎症和凋亡途径后对神经胶质细胞损伤的保护作用。对照组不做任何处理，HO 组用 0.5 mM HO 处理 24 小时。卡托普利组用不同浓度的卡托普利处理 24 小时。卡托普利+HO 组先用卡托普利预处理 1 小时，然后暴露于 0.5 mM HO 24 小时。在卡托普利+HO 组中，所有浓度的卡托普利均显著提高 C6 细胞的细胞活力。它还显著增加了 TAS 并降低了 TOS 水平，这是氧化应激的一个指标。此外，卡托普利显著降低了炎症标志物，包括 NF-kB、IL-1β、COX-1 和 COX-2 水平。流式细胞术结果还表明，卡托普利预处理可显著降低细胞凋亡率。此外，卡托普利可显著降低促凋亡 Bax 蛋白水平并提高抗凋亡 Bcl-2 蛋白水平。总之，卡托普利通过抑制氧化应激、炎症和凋亡对 HO 诱导的氧化损伤后的 C6 细胞具有保护作用。然而，需要进一步的研究来评估卡托普利作为神经保护剂的潜力。
