Yiangou M, Konidaris C, Victoratos P, Hadjipetrou-Kourounakis L
Faculty of Sciences, School of Biology, Department of Genetics, Development and Molecular Biology, Aristotle University of Thessaloniki, Greece.
Clin Exp Immunol. 1993 Oct;94(1):156-62. doi: 10.1111/j.1365-2249.1993.tb05994.x.
Honey bee venom (HBV) administration to adjuvant arthritic (AA) rats resulted in a significant suppression of arthritis and in suppression of the hepatic acute phase alpha 1-acid glycoprotein (AGP) gene induction at the early stages of disease development. AGP administration in AA rats resulted in acceleration of arthritis development and in increase of severity and duration of the disease. IL-1, IL-6, tumour necrosis factor (TNF) and glucocorticoids alone are not responsible for the HBV-mediated AGP gene down-regulation. These results indicate that AGP gene expression in AA and HBV-treated AA rats involves the interaction of several factors, and that AGP plays a role for AA development in rats.
给佐剂性关节炎(AA)大鼠注射蜜蜂毒液(HBV),在疾病发展的早期阶段可显著抑制关节炎,并抑制肝脏急性期α1-酸性糖蛋白(AGP)基因的诱导。给AA大鼠注射AGP会导致关节炎发展加速,疾病严重程度和持续时间增加。单独的白细胞介素-1、白细胞介素-6、肿瘤坏死因子(TNF)和糖皮质激素并不负责HBV介导的AGP基因下调。这些结果表明,AA大鼠和HBV处理的AA大鼠中AGP基因的表达涉及多种因素的相互作用,并且AGP在大鼠AA的发展中起作用。