The effects of lithium gamma-linolenic acid in reversing LPBM5 MuLV induced suppression of hematopoietic progenitor cells in vitro.

O R Oakley, N K Hughes, N J Birch, M L Winther, D F Horrobin, V S Gallicchio
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Abstract

Lithium gamma linolenic acid (Li-GLA), was evaluated for its possible role as an antiviral agent. Li-GLA 15 micrograms ml-1 was administered to both normal and LP-BM5 MuLV retroviral infected murine bone marrow cultures. After 2 weeks of treatment, numbers of progenitors being produced by infected/treated cultures were reduced to some 10% that of normal cultures. In the remaining 4 weeks, numbers of CFU-GM and BFU-E hematopoietic progenitors returned within normal range. The efficacy of Li-GLA in relieving retroviral hematopoietic bone marrow suppression correlates to a reduction in interleukin-4 (IL-4) secretion, normally elevated in association with LP-BMP5 infection. These data indicate that this reduction in bone marrow suppression of LP-BMP5 infected cells may be due to a killing of infected cells by the Li-GLA, rather than stimulating hematopoiesis as with other lithium compounds. To conclude this may indicate the possible dual effect of administration of LiGLA to virally infected individuals in reducing viral titre and to lower the toxicities associated with long term drug therapy.

锂-亚麻酸在体外逆转LPBM5 MuLV诱导的造血祖细胞抑制中的作用。
锂γ -亚麻酸(Li-GLA),评估其作为抗病毒药物的可能作用。Li-GLA 15微克ml-1被给予正常和LP-BM5感染的小鼠骨髓培养物。治疗2周后,感染/处理培养物产生的祖细胞数量减少到正常培养物的10%左右。在剩余的4周内,CFU-GM和BFU-E造血祖细胞数量恢复到正常范围。Li-GLA缓解逆转录病毒造血骨髓抑制的功效与白细胞介素-4 (IL-4)分泌的减少有关,白细胞介素-4的分泌通常与LP-BMP5感染有关。这些数据表明,LP-BMP5感染细胞骨髓抑制的减少可能是由于Li-GLA杀死了感染细胞,而不是像其他锂化合物那样刺激造血。总之,这可能表明对病毒感染个体施用LiGLA在降低病毒滴度和降低与长期药物治疗相关的毒性方面可能具有双重作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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