Nimodipine is a 1,4-dihydropyridine L-type calcium channel antagonist, mainly used to treat aneurysmal subarachnoid hemorrhage (aSAH) and prevent cerebral vasospasm[1]. Nimodipine can block voltage-dependent calcium channels, reduce calcium influx, protect neurons, and reduce oxidative stress and cell apoptosis[2, 3].
In vitro, pretreatment of PC12 cells with Nimodipine (20μM) for 48h significantly reduced the cytotoxic effects of EtOH and osmotic stress on cells, but had no effect on hypoxia-induced cytotoxicity[4]. Pretreatment of Schwann cells, neurons and astrocytes with Nimodipine (1, 10, 20μM) for 24h reduced the cytotoxic effects of EtOH, osmotic pressure and heat stress on cells in a dose-dependent manner[5].
In vivo, Nimodipine (5, 10, 15mg/kg) was intraperitoneally injected into rats with experimental myocardial infarction for 7 days, which improved the hemodynamic parameters of rats, reversed the histopathological and ultrastructural changes, increased endogenous antioxidants, maintained the serum levels of myocardial biomarkers CK-MB, LDH, SGOT, Trop-T and cGMP, and showed a more powerful cardioprotective effect when combined with vinpocetine[6].
References:
[1] Wiputri O I, Hidayati H B. The Role of Nimodipine as a Neurorestorative Drug in Preventing Cerebral Vasospasm Related to Subarachnoid Aneurysmal Hemorrhage[J]. Int J Pharma Res Health Sci, 2019, 7(6): 3079-83.
[2] Singh A, Verma P, Balaji G, et al. Nimodipine, an L-type calcium channel blocker attenuates mitochondrial dysfunctions to protect against 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-induced Parkinsonism in mice[J]. Neurochemistry international, 2016, 99: 221-232.
[3] Kusakabe M, Hasegawa Y. Nimodipine promotes neurite outgrowth and protects against neurotoxicity in PC12 cells[J]. Iranian journal of basic medical sciences, 2021, 24(1): 51.
[4] Bork K, Wurm F, Haller H, et al. Neuroprotective and neuroregenerative effects of nimodipine in a model system of neuronal differentiation and neurite outgrowth[J]. Molecules, 2015, 20(1): 1003-1013.
[5] Leisz S, Simmermacher S, Prell J, et al. Nimodipine-dependent protection of schwann cells, astrocytes and neuronal cells from osmotic, oxidative and heat stress is associated with the activation of AKT and CREB[J]. International Journal of Molecular Sciences, 2019, 20(18): 4578.
[6] Ansari M A, Iqubal A, Ekbbal R, et al. Effects of nimodipine, vinpocetine and their combination on isoproterenol-induced myocardial infarction in rats[J]. Biomedicine & Pharmacotherapy, 2019, 109: 1372-1380.
Nimodipine是一种1,4-二氢吡啶类L型钙离子通道拮抗剂，主要用于治疗动脉瘤性蛛网膜下腔出血（aSAH），预防脑血管痉挛[1]。Nimodipine能够阻断电压依赖性钙通道，减少钙离子内流，对神经元具有保护作用，还能够减轻氧化应激和细胞凋亡[2, 3]。
在体外，Nimodipine（20μM）预处理PC12细胞48h，显著降低了EtOH和渗透压应激条件对细胞的细胞毒性作用，而对缺氧诱导的细胞毒性无影响[4]。Nimodipine（1, 10, 20μM）预处理Schwann细胞、神经元细胞和星形胶质细胞24h，以剂量依赖性方式降低了EtOH、渗透压和热应激条件对细胞的细胞毒性作用[5]。
在体内，Nimodipine（5, 10, 15mg/kg）通过腹腔注射治疗实验性心肌梗死大鼠7天，改善了大鼠血液动力学参数，逆转了组织病理学和超微结构的变化，增加了内源性抗氧化剂，维持了心肌生物标志物CK-MB、LDH、SGOT、Trop-T和cGMP的血清水平，且与Vinpocetine联合用药表现出了更强大的心脏保护作用[6]。