纳米硒抗胰岛β细胞凋亡作用与机制的研究

Effect and Mechanism of Selenium Nanoparticle Against Islet β Cell Apoptosis

旨在研究纳米硒(Se NPs)抗二型糖尿病胰岛β细胞凋亡的作用及机制。通过电子显微镜,纳米粒度仪等技术方法对Se NPs的表征进行鉴定,并运用相关分子生物学技术验证其对于胰岛β细胞凋亡模型的保护作用及机制。结果表明,壳聚糖(CS)修饰后的Se NPs表面电荷增加到24.8 mv,其保存期延长到100 d以上。另外,细胞学实验表明浓度在2μmol/L以下Se NPs不具有毒性,38.1 nmol/L Se NPs可通过激活硫氧还蛋白还原酶(Trx R)活性,从而减轻胞内氧化应激(ROS)水平,最终使胰岛β凋亡模型细胞存活率提高了31.75%。动物学实验也表明Se NPs能抗胰岛β细胞凋亡。因此,Se NPs可有效减轻二型糖尿病中胰岛β细胞凋亡,对于二型糖尿病具有潜在的治疗价值。

The purpose of this research was to study the effect and molecular mechanism of selenium nanoparticles（Se NPs）in thetreatment of islet β cell apoptosis in type 2 diabetes mellitus. Electron microscope and nanoparticle size analyzer were used to identify Se NPssurface morphology,and relevant molecular biological techniques were used to validate the protection effect and mechanism of Se NPs on isletβ cells apoptotic model. Results showed that the surface charge of selenium nanoparticle decorated by chitosan（CS）increased to 24.8 mv,and its storage time was extended to over 100 days. Cytology results showed that Se NPs under 2 μmol/L had no toxicity. Meanwhile,Se NPs in38.1 nmol/L activated Trx R activity and reduced intracellular ROS level,which led to apoptotic model cells survival rate significantly increased31.75%. Furthermore,the animal experiments also verified that Se NPs could resist the apoptosis of islet cell β. In conclusion,Se NPs mayeliminate the apoptosis of islet cell β in type 2 diabetes mellitus,which shows a potential therapeutic activity in the treatment of type 2 diabetes.