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作 者:王芳[1] 卢欣烁 李岩[2] 董晓婷[1] 杨杰波 刘方芳[2] 金瑶[2] 李明[1]
机构地区:[1]广东药科大学基础学院,广东广州510006 [2]广州中医药大学基础医学院,广东广州510006
出 处:《广东药科大学学报》2017年第2期207-210,230,共5页Journal of Guangdong Pharmaceutical University
基 金:广东省科技计划项目(2014A020212266;2016A020215156);广州中医药大学薪火计划项目(XH20150101)
摘 要:目的观察丹参酮ⅡA磺酸钠(STS)对PM2.5引起的血管内皮细胞EA.hy926损伤的保护作用。方法取对数生长期EA.hy926细胞分为对照组、100μg/mL PM2.5组及STS干预组(先给予12.5、25、50μg/mL STS干预后再加入100μg/mL PM2.5)。24 h后CCK8法测定细胞的存活率,荧光标记法检测细胞内氧自由基生成情况,流式细胞术检测细胞凋亡率,Western blot法检测凋亡蛋白酶Caspase-9和Caspase-3的表达变化。结果 PM2.5对EA.hy926细胞有明显的毒性,可以导致细胞内氧自由基生成增多,并引起Caspase-9和Caspase-3活化造成细胞凋亡,与对照组比较差异有统计学意义;STS可以抑制PM2.5对EA.hy926细胞的毒性,降低胞内活性氧(ROS)生成及Caspase-9和Caspase-3的活化,减少细胞凋亡数目,与PM2.5组比较差异有统计学意义。结论丹参酮ⅡA磺酸钠可以减少PM2.5引起的血管内皮细胞凋亡,其保护作用可能与抑制氧自由基生成有关。Objective To investigate the protective effect of sodium Tanshinone 11 A sulfonate (STS) on EA. hy926 cells exposed to PM2.5. Methods Endothelial cell line EA.hy926 was cultured in vitro and exposed to 100μg/mL PM2.5 with or without different concentrations of STS ( 12.5, 25, 50 μg/mL). After 24 h the cell viability was measured by CCK-8 kit and the generation of intracellular ROS was measured with DCFH- DA. Cell apoptosis was detected by flow cytometry with Annexin V-FITC/PI staining and the activity of Caspase 9 and Caspase 3 was detected by Western blot. Results Compared with the control group, PM2.5 decreased endothelial cell viability, increased intracellular production of ROS, induced cell apoptosis and upregulated the activation of Caspase 9 and Caspase 3. After pretreatment with STS, the viability of EA.hy926 cells was increased markedly and the generation of ROS was decreased. The cell apoptosis was also inhibited by STS treatment followed by downregulation of Caspase 9 and Caspase 3. Conclusion STS could protect vascular endothelial ceils bv reducing oxidative stress and cell atm-tosis induced bv PM2.5.
关 键 词:丹参酮ⅡA磺酸钠 PM2.5 EA.hy926细胞 氧化应激 凋亡
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