Fu Hui-ni, Wu Li, Duan Lian-wen, Lü Shu-zhi
Yao Xue Xue Bao. 2017 Mar;52(3):468-73.
Inhibition of apoptosis induced by oxidative stress is an effective way to reduce myocardial injury. In this study, we used H2O2-stimulated rat cardiac myoblast cell line (H9c2) as an oxidative damage model. Curcumin (Cur) was chosen as a model drug and mesoporous silica nanoparticles (MSNs) were chosen as the carrier to construct a Cur-loaded delivery system (Cur@MSNs) and to examine its protective effects against oxidative damage. The MSNs guaranteed efficient loading and controlled release of Cur. Besides, the hydrophilicsilanol groups on the surface of MSNs promoted the Cur solubility in water and increased its cellular uptake amount, which improved the bioavailability of Cur. The results suggest that the Cur@MSNs was pharmacologically active in the reduction of the oxidative damage of H9c2 cells. It was verified that a great decrease of reactive oxygen species was inducted by Cur@MSNs, which led to the protective effects against oxidative damage.
抑制氧化应激诱导的细胞凋亡是减轻心肌损伤的有效途径。在本研究中，我们使用H2O2刺激的大鼠心肌成肌细胞系（H9c2）作为氧化损伤模型。选择姜黄素（Cur）作为模型药物，选择介孔二氧化硅纳米颗粒（MSNs）作为载体，构建负载Cur的递送系统（Cur@MSNs），并研究其对氧化损伤的保护作用。MSNs保证了Cur的高效负载和控释。此外，MSNs表面的亲水性硅醇基团促进了Cur在水中的溶解度并增加了其细胞摄取量，从而提高了Cur的生物利用度。结果表明，Cur@MSNs在减轻H9c2细胞氧化损伤方面具有药理活性。证实Cur@MSNs可诱导活性氧的大幅减少，从而产生对氧化损伤的保护作用。
