Captopril is an orally active angiotensin-converting enzyme (ACE) inhibitor with an IC50 value of 0.025μM[1]. Captopril exerts its effects by blocking the conversion of angiotensin I to angiotensin II, thereby achieving vasodilation, lowering blood pressure, and reducing cardiac workload[2]. Captopril is commonly used in the treatment and research of hypertension, heart failure, and diabetic nephropathy[3,4].
In vitro, BV2 microglial cells were incubated with Captopril (0.1, 0.3, 1, and 3mM) and lipopolysaccharide (LPS, 7ng/mL) for 24h. Low concentrations of Captopril (0.3, 1mM) enhanced LPS-induced NO production, whereas a high concentration of Captopril (3mM) inhibited LPS-induced NO production[5].
In vivo, normal ICR mice were treated with Captopril (10mg/kg) by gavage for 8 weeks, resulting in decreased mean arterial pressure and serum calcium levels, as well as increased urinary calcium excretion[6]. BALB-c mice were pretreated with Captopril (25, 50mg/kg) via intraperitoneal injection for 7 days. On day 7, 30min after the last dose, pentylenetetrazole (PTZ, 60mg/kg) was injected to induce epileptic seizures. Captopril treatment significantly reduced the formation of dark neurons in the hippocampal CA1, CA2, CA3 regions and the dentate gyrus (DG)[7].
References:
[1] Afrin S, Rakib M A, Kim B H, et al. Eritadenine from edible mushrooms inhibits activity of angiotensin converting enzyme in vitro[J]. Journal of Agricultural and Food Chemistry, 2016, 64(11): 2263-2268.
[2] Bolterman R J, Manriquez M C, Ruiz M C O, et al. Effects of captopril on the renin angiotensin system, oxidative stress, and endothelin in normal and hypertensive rats[J]. Hypertension, 2005, 46(4): 943-947.
[3] Atkinson A B, Robertson J I S. Captopril in the treatment of clinical hypertension and cardiac failure[J]. The Lancet, 1979, 314(8147): 836-839.
[4] Heel R C, Brogden R N, Speight T M, et al. Captopril: a preliminary review of its pharmacological properties and therapeutic efficacy[J]. Drugs, 1980, 20(6): 409-452.
[5] Asraf K, Torika N, Apte R N, et al. Microglial activation is modulated by captopril: in vitro and in vivo studies[J]. Frontiers in Cellular Neuroscience, 2018, 12: 116.
[6] Yang M, Xia C, Song Y, et al. Impairing effects of angiotensin-converting enzyme inhibitor captopril on bone of normal mice[J]. European Journal of Pharmacology, 2016, 771: 40-47.
[7] Tastemur Y, Gumus E, Ergul M, et al. Positive effects of angiotensin-converting enzyme (ACE) inhibitor, captopril, on pentylenetetrazole-induced epileptic seizures in mice[J]. Tropical Journal of Pharmaceutical Research, 2020, 19(3): 637-643.
Captopril是一种具有口服活性的血管紧张素转化酶（ACE）抑制剂，IC50值为0.025μM[1]。Captopril通过阻断血管紧张素I转化为血管紧张素II，达到舒张血管、降低血压和减轻心脏负荷的效果[2]，通常用于高血压、心力衰竭及糖尿病肾病等的治疗和研究[3,4]。
在体外，Captopril（0.1, 0.3, 1, and 3mM）和脂多糖（LPS, 7ng/mL）与小胶质细胞BV2共培养24h，低浓度Captopril（0.3, 1mM）增强LPS诱导的NO产生，而高浓度Captopril（3mM）抑制LPS诱导的NO产生[5]。
在体内，Captopril（10mg/kg）通过灌胃处理正常ICR小鼠8周，小鼠平均动脉压和血清钙降低，尿钙增加[6]。Captopril（25, 50mg/kg）通过腹腔注射预处理BALB-c小鼠7天，第7天给药30min后注射pentylenetetrazole（PTZ, 60mg/kg）诱导癫痫发作，Captopril处理可显著减少海马CA1、CA2、CA3区和齿状回（DG）的暗神经元形成[7]。