Carbon monoxide releasing molecule-2 (CORM-2) exhibited protection against cardiac hypoxia reoxygenation injury (H/R). However, its poor water solubility and short half-life restrict its clinical usage. The present study aims to investigate whether encapsulation of CORM-2 in mesoporous silica (MSN-A-CORM-2) can enhance its anti-H/R effect in cardiac cell lines H9C2 (cardiomyoblast) and 3T3 (fibroblast). Mesoporous silica nanoparticles (MSN) were synthesized by co-operative self-assembly technique through solvothermal strategy and terminated with amine functional groups (MSN-A). The ligand, CORM-2, was linked to the terminal amine group in mesoporous silica. The physicochemical characterization of the compound was made by using SEM, TEM, FTIR, and EDS analysis. Further, we evaluated the biological effect of MSN-A-CORM-2 against H/R in H9C2 and 3T3 cells. The results demonstrated that MSN-A-CORM-2 was less toxic as compared to that of standard CORM-2. The comparable potential of CORM-2 in combating H/R got enhanced upon encapsulation with mesoporous silica.

一氧化碳释放分子 2 (CORM-2) 表现出对心脏缺氧再氧合损伤 (H/R) 的保护作用。然而，其水溶性差和半衰期短限制了其临床应用。本研究旨在研究将 CORM-2 封装在介孔二氧化硅 (MSN-A-CORM-2) 中是否可以增强其在心肌细胞系 H9C2（心肌细胞）和 3T3（成纤维细胞）中的抗 H/R 作用。介孔二氧化硅纳米粒子（MSN）是通过溶剂热策略通过协同自组装技术合成的，并以胺官能团（MSN-A）为末端。配体 CORM-2 与介孔二氧化硅中的末端胺基连接。通过使用SEM、TEM、FTIR和EDS分析对化合物进行了理化表征。更远，我们在 H9C2 和 3T3 细胞中评估了 MSN-A-CORM-2 对 H/R 的生物学效应。结果表明，与标准 CORM-2 相比，MSN-A-CORM-2 的毒性较小。用介孔二氧化硅封装后，CORM-2 在对抗 H/R 方面的可比潜力得到了增强。