氧化低密度脂蛋白诱导血管平滑肌细胞凋亡及其分子学机制研究

目的 研究氧化低密度脂蛋白（Ox-LDL）诱导血管平滑肌细胞（VSMCs）凋亡的机制。方法 采用电镜观察、Hoechst33342染色、Western blotting 印迹分析法研究Ox-LDL诱导VSMCs凋亡的效应及其分子学机制。结果 Ox-LDL作用VSMCs 24 h后,电镜下VSMCs出现凋亡的形态学特征：细胞核固缩、凋亡小体形成;Hoechest33342染色可见,凋亡的细胞核或细胞质内出现浓染致密的块状或颗粒状荧光;Western blotting结果显示,p53蛋白含量升高,而Bcl-2蛋白含量降低。结论 Ox-LDL 能诱导大鼠VSMCs 凋亡,并呈现一定的浓度和时间依赖关系;p53和bcl-2基因在Ox-LDL诱导的VSMCs凋亡中可能发挥重要的调控作用。

Induction of apoptosis in vascular smooth muscle cells by oxidized low-density lipoprotein and its molecular mechanism

Objective To investigate the apoptosis of vascular smooth muscle cells (VSMCs) of rats induced by oxidized low-density lipoprotein (Ox-LDL) and explore its molecular mechanism. Method Electron microscopy, Hoechst 33342 staining assay and Western blotting were performed to study Ox-LDL-induced apoptosis in rat VSMCs. Results VSMCs treated with Ox-LDL for 24 h showed typical apoptotic changes: cell shrinkage, cytoplasm and chromatin condensation, observed electromicroscopically. Hoechest 33342 staining assay showed thick granulated fluorescence in condensed nuclei and cytoplasm, and apoptotic bodies was also visible. Western blotting demonstrated that p53 protein level increased and Bcl-2 protein level decreased when apoptosis occurred. Conclusions Ox-LDL can induce apoptosis in VSMCs in dose- and concentration-dependent manner. The expression of p53, acting to induce apoptosis, was increased, while that of Bcl-2, inhibitor of apoptosis,was decreased and altered expressions of p53 and bcl-2 gene possibly play an important role in regulating Ox-LDL-induced apoptosis.