Zhang Xiao-Dan, Zhao Shu-Ya, Li Yun-Lin, Zhu Da-Ling, Zhang Ru, Sheng Jie-Jing, Wang Shu-Jing
Pharmaceutical College, Harbin University of Commerce, Harbin 150000, China.
College of Pharmacy, Harbin Medical University, Daqing 163000, China.
Zhongguo Zhong Yao Za Zhi. 2017 Jun;42(12):2350-2354. doi: 10.19540/j.cnki.cjcmm.2017.0112.
To investigate the effect of taurine(Tau) on ICAM-1, VCAM-1 by p-p38 pathway in bovine pulmonary artery endothelial cells(PAECs) and explore its mechanism of action. Generation 4-12 cells in primary cultures of PAECs were used in experiments and divided into five groups： control group, hypoxia(hyp) group, inhibitor(SB203580) group, treatment(Tau) group, and treatment+inhibitor(SB+Tau) group. The concentration of Tau：100 mmol•L⁻¹; p38 inhibitor SB203580： 20 μmol•L⁻¹; and the treatment time was 12 h. MTT assay was used to detect the inhibitory effect of different concentrations of Tau on PAECs. Western blot and Real-time PCR method were used to detect the p38 pathway proteins and ICAM-1, VCAM-1 expression levels. Immunofluorescence was used to investigate p38 nuclear displacement situation. The results of MTT showed that the inhibitory effect was gradually increased with increasing concentrations of Tau. Western blot and RT-PCR revealed that the protein and mRNA expression levels of ICAM-1, VCAM-1 were reduced by Tau. Western blot and immunofluorescence showed Tau can inhibit p38 activation. Tau may decrease the expression levels of VCAM-1 and ICAM-1 in endothelial cells induced by hypoxia through MAPK p38 pathway.
探讨牛肺动脉内皮细胞（PAECs）中牛磺酸（Tau）通过p-p38途径对细胞间黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1）的影响，并探索其作用机制。采用原代培养的第4-12代PAECs进行实验，分为五组：对照组、缺氧（hyp）组、抑制剂（SB203580）组、处理（Tau）组和处理+抑制剂（SB+Tau）组。Tau浓度为100 mmol•L⁻¹；p38抑制剂SB203580为20 μmol•L⁻¹；处理时间为12 h。采用MTT法检测不同浓度Tau对PAECs的抑制作用。采用蛋白质印迹法和实时荧光定量PCR法检测p38途径蛋白以及ICAM-1、VCAM-1的表达水平。采用免疫荧光法研究p38核转位情况。MTT结果显示，随着Tau浓度升高，抑制作用逐渐增强。蛋白质印迹法和RT-PCR结果显示，Tau可降低ICAM-1、VCAM-1的蛋白和mRNA表达水平。蛋白质印迹法和免疫荧光结果显示，Tau可抑制p38激活。Tau可能通过丝裂原活化蛋白激酶p38途径降低缺氧诱导的内皮细胞中VCAM-1和ICAM-1的表达水平。
