CA 074

CA-074是一种特异性组织蛋白酶B抑制剂，可消除Abeta42活化的BV2细胞引起的神经毒性效应[1]。经组织蛋白酶B抑制剂CA-074 或者Z-FA-FMK处理的培养基可抑制TPA抑制细胞生长的作用以及尿激酶原的活化[2]。CA-074给药可抑制对外源性抗原的反应，如乙肝病毒抗原、卵白蛋白和硕大利什曼原虫抗原，并诱导辅助T细胞反应的转换，CD4+ T细胞从Th2细胞转变为Th1细胞，从而下调IgE和IgG1的产生[3]。

在catB(+/+)小鼠中，CA-074 Me通过药理学抑制组织蛋白酶B，可减少肿瘤坏死因子α（TNF-α）诱导的肝损伤[4]。

组织蛋白酶B抑制剂E-64、CA-074和vitamin B6可强烈抑制Th-2型免疫反应。

参考文献：
[1] Identification of cathepsin B as a mediator of neuronal death induced by Abeta-activated microglial cells using a functional genomics approach.  Gan, L., Ye, S., Chu, A., Anton, K., Yi, S., Vincent, V.A., von Schack, D., Chin, D., Murray, J., Lohr, S., Patthy, L., Gonzalez-Zulueta, M., Nikolich, K., Urfer, R. J. Biol. Chem. (2004)
[2] Phorbol ester activation of a proteolytic cascade capable of activating latent transforming growth factor-betaL a process initiated by the exocytosis of cathepsin B.  Guo, M., Mathieu, P.A., Linebaugh, B., Sloane, B.F., Reiners, J.J. J. Biol. Chem. (2002)
[3] Insights into the roles of cathepsins in antigen processing and presentation revealed by specific inhibitors.  Katunuma, N., Matsunaga, Y., Himeno, K., Hayashi, Y. Biol. Chem. (2003)
[4] Cathepsin B knockout mice are resistant to tumor necrosis factor-alpha-mediated hepatocyte apoptosis and liver injury: implications for therapeutic applications.  Guicciardi, M.E., Miyoshi, H., Bronk, S.F., Gores, G.J. Am. J. Pathol. (2001)