Li Fang, Mei Yunhua, Wang Ying, Chen Chunhua, Tu Jianglong, Xiao Baoguo, Xu Lingyun
Joint Immunology Laboratory of Institute of Health Sciences and Shanghai Institute of Immunology, Shanghai Institutes for Biological Sciences/Chinese Academy of Sciences, and Shanghai Second Medical University, Shanghai 200025, China.
Cell Immunol. 2005 Mar;234(1):23-30. doi: 10.1016/j.cellimm.2005.04.015.
Trichosanthin (TCS) has been found to exhibit inflammation-suppressing effect but the underlying mechanisms are not clear. In this study, we found that TCS inhibited OVA-specific T cell proliferation in a dose-dependent manner. Such inhibition was correlated with enhanced cell death. At the same time, inducible nitric oxide synthase (iNOS) mRNA expression and protein levels were found increased in cells treated with TCS, and nitric oxide (NO) production by cells was elevated in the presence of TCS. When L-NIL, the specific inhibitor of iNOS, was added to suppress NO production induced by TCS, OVA-specific cell death was significantly inhibited, meanwhile, thymidine incorporation of cells was rescued towards normal levels. These results indicate that TCS could inhibit antigen-specific T cell activation via NO-mediated apoptosis pathway.
天花粉蛋白（TCS）已被发现具有抗炎作用，但其潜在机制尚不清楚。在本研究中，我们发现TCS以剂量依赖的方式抑制卵清蛋白（OVA）特异性T细胞增殖。这种抑制作用与细胞死亡增加相关。同时，在用TCS处理的细胞中，诱导型一氧化氮合酶（iNOS）的mRNA表达和蛋白水平均升高，并且在TCS存在的情况下细胞产生的一氧化氮（NO）增加。当加入iNOS的特异性抑制剂L-NIL以抑制TCS诱导的NO产生时，OVA特异性细胞死亡被显著抑制，同时，细胞的胸苷掺入恢复到正常水平。这些结果表明，TCS可通过NO介导的凋亡途径抑制抗原特异性T细胞活化。
