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抑制氧化应激诱导的心肌细胞凋亡是减轻心肌损伤的有效途径。本研究以乳鼠心肌细胞系H9c2为模型细胞,建立体外心肌细胞过氧化氢(H_2O_2)氧化损伤模型。以介孔氧化硅纳米粒(MSNs)为药物载体,姜黄素(Cur)为模型药物,构建负载Cur的纳米药物控释系统(Cur@MSNs)。研究Cur@MSNs对心肌细胞氧化应激损伤的作用。MSNs独特的介孔孔道结构可以实现对Cur的高效负载及缓慢释放,MSNs表面的亲水硅羟基可以改善Cur的水溶性,增加细胞对Cur的摄取量,提高难溶性Cur的生物利用度。体外细胞实验发现,Cur@MSNs中Cur保持了良好的药理活性,且可以明显减弱H_2O_2诱发的心肌细胞氧化损伤。体外细胞毒性机制研究发现,Cur@MSNs可明显降低H_2O_2氧化损伤产生的活性氧自由基含量,从而对心肌细胞损伤起到保护作用。
Inhibition of oxidative stress-induced cardiomyocyte apoptosis is an effective way to reduce myocardial injury. In this study, neonatal rat cardiomyocyte cell line H9c2 was used as a model cell to establish a model of oxidative damage of hydrogen peroxide (H 2 O 2) in cardiomyocytes in vitro. Using curcumin (Cur) as a model drug, mesoporous silica nanoparticles (MSNs) as a drug carrier were used to construct Cur loaded drug delivery system. To investigate the effect of Cur @ MSNs on oxidative stress injury in cardiomyocytes. MSNs unique mesoporous pore structure can achieve high efficiency and slow release of Cur. The hydrophilic silanols on MSNs can improve the water solubility of Cur, increase the uptake of Cur and increase the bioavailability of Cur. In vitro experiments showed that Cur maintained a good pharmacological activity in Cur @ MSNs and markedly attenuated H 2 O 2 -induced cardiomyocyte oxidative damage. In vitro cytotoxicity mechanism study found that Cur @ MSNs can significantly reduce the oxidative H_2O_2 oxidative damage generated by reactive oxygen free radicals, which play a protective effect on myocardial cell injury.