Migliorati G, D'Adamio L, Coppi G, Nicoletti I, Riccardi C
Institute of Pharmacology, Perugia University Medical School, Italy.
Immunopharmacol Immunotoxicol. 1992;14(4):737-48. doi: 10.3109/08923979209009231.
Experiments were performed to analyze the possible effect of the immunomodulating agent Pidotimod (3-L-pyroglutamyl-L-thiazolidine-4-carboxylic acid) on mouse Natural Killer (NK) cell activity and glucocorticoid hormone(GCH)-induced thymocyte apoptosis. The results indicate that in vivo treatment with Pidotimod (200 mg/Kg ip for 5 days) causes a significant increase in NK activity and in vitro treatment produces a significant reduction of dexamethasone-induced thymocyte apoptosis. This inhibition appears to be dose-dependent and is also evident against TPA or Ca(++)ionophore-induced apoptosis.
进行实验以分析免疫调节剂匹多莫德（3-L-焦谷氨酸-L-噻唑烷-4-羧酸）对小鼠自然杀伤（NK）细胞活性和糖皮质激素（GCH）诱导的胸腺细胞凋亡的可能影响。结果表明，体内给予匹多莫德（200mg/Kg腹腔注射，共5天）可使NK活性显著增加，体外给予可显著减少地塞米松诱导的胸腺细胞凋亡。这种抑制作用似乎呈剂量依赖性，对TPA或钙离子载体诱导的凋亡也很明显。
