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匹多莫德刺激自然杀伤细胞活性并抑制胸腺细胞死亡。

Pidotimod stimulates natural killer cell activity and inhibits thymocyte cell death.

作者信息

Migliorati G, D'Adamio L, Coppi G, Nicoletti I, Riccardi C

机构信息

Institute of Pharmacology, Perugia University Medical School, Italy.

出版信息

Immunopharmacol Immunotoxicol. 1992;14(4):737-48. doi: 10.3109/08923979209009231.

Abstract

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.

摘要

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。

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