Department of Pharmacy, Practice & Clinical Pharmacy, Faculty of Pharmacy, Future University, Cairo, Egypt.
Department of Medical Pharmacology, Faculty of Medicine, Cairo University, Cairo, Egypt.
Curr Pharm Biotechnol. 2024;25(6):772-786. doi: 10.2174/0113892010256434231010062233.
Acute myocardial infarction (AMI) is the most prevalent cause of myocardial fibrosis and the leading cause of mortality from cardiovascular disease. The goal of this work was to synthesize Balanites aegyptiaca oil-silver nanoparticles (BAO-Ag-NPs) and evaluate their cardioprotective effect against ISO-induced myocardial infarction in rats, as well as their mechanism.
BAO was isolated, and the unsaturated fatty acids were estimated. BAO-Ag-NPs was prepared, LD50 was calculated to evaluate its cardioprotective activity against ISO (85 mg/kg)-induced AMI. Different doses of BAO-Ag-NPs (1/50 LD50; 46.6 mg/kg.b.w and 1/20 LD50; 116.5 mg) were received to the rats.
The total fatty acids and unsaturated fatty acids generated by BAO were 909.63 and 653.47 mg/100 g oil, respectively. Oleic acid methyl ester, 9-octadecenoic acid methyl ester, and 9, 12-Octadecadienoic acid methyl ester were the predominant ingredients, with concentrations of 107.6, 243.42, and 256.77 mg/100 g oil, respectively. According to TEM and DLS examinations, BAO-Ag-NPs have a size of 38.20 ± 2.5 nm and a negative zeta potential of -19.82 ± 0.30 mV, respectively. The LD50 of synthesized BAO-Ag-NPs is 2330 mg. On the other hand, BAOAg- NPs reduce myocardial necrosis by lowering increased BNP, cTnI, CK-MB, TC, TG, MDA, MMP2, TGF-β1, PGE2, and IL-6 levels. Furthermore, BAO-Ag-NPs inhibit the expression of ET-1, ICAM-1, and VCAM-1 genes as well as enhance HDL-C, CAT, and GSH levels when compared to the ISO-treated group of rats. Histopathological findings suggested that BAO-Ag- NPs enhance cardiac function by increasing posterior wall thickness in heart tissues.
BAO-Ag-NPs protect against AMI in vivo by regulating inflammation, excessive autophagy, and oxidative stress, as well as lowering apoptosis via suppression of the ET-1, ICAM-1, and VCAM-1 signaling pathways.
急性心肌梗死（AMI）是心肌纤维化最常见的原因，也是心血管疾病死亡的主要原因。本研究旨在合成乳木果油-银纳米粒子（BAO-Ag-NPs），并评价其对 ISO 诱导的大鼠心肌梗死的心脏保护作用及其机制。
分离乳木果油，估算不饱和脂肪酸。制备 BAO-Ag-NPs，计算 LD50 以评估其对 ISO（85mg/kg）诱导的 AMI 的心脏保护活性。不同剂量的 BAO-Ag-NPs（1/50 LD50；46.6mg/kg.b.w 和 1/20 LD50；116.5mg）给予大鼠。
BAO 产生的总脂肪酸和不饱和脂肪酸分别为 909.63 和 653.47mg/100g 油。油酸甲酯、9-十八碳烯酸甲酯和 9,12-十八碳二烯酸甲酯是主要成分，浓度分别为 107.6、243.42 和 256.77mg/100g 油。根据 TEM 和 DLS 检查，BAO-Ag-NPs 的粒径为 38.20±2.5nm，zeta 电位为-19.82±0.30mV。合成的 BAO-Ag-NPs 的 LD50 为 2330mg。另一方面，BAO-Ag-NPs 通过降低升高的 BNP、cTnI、CK-MB、TC、TG、MDA、MMP2、TGF-β1、PGE2 和 IL-6 水平来减轻心肌坏死。此外，与 ISO 处理组大鼠相比，BAO-Ag-NPs 抑制 ET-1、ICAM-1 和 VCAM-1 基因的表达，并提高 HDL-C、CAT 和 GSH 水平。组织病理学检查结果表明，BAO-Ag-NPs 通过增加心脏组织后壁厚度来增强心脏功能。
BAO-Ag-NPs 通过调节炎症、过度自噬和氧化应激，以及通过抑制 ET-1、ICAM-1 和 VCAM-1 信号通路降低细胞凋亡，来防止体内 AMI。
