摘要
目的研究人类重组白介素2（rIL-2）对培养大鼠心肌细胞产生一氧化氮（NO）及线粒体活性的影响。方法在培养心肌细胞时分别或同时加入rIL-2、单甲基L-精氨酸（L-NMMA）以及L-精氨酸（L-Arg），并测定培养液中NO浓度，心肌细胞内的线粒体活性值。结果心肌细胞加rIL-2培养48h与对照组相比NO产生显著增加[（85±6.1）比（10±2.5）nmol·（106细胞）-1，P＜0.01]。rIL-2刺激NO产生呈时间（6～48h）和剂量（5×104～1×106IU·L-1）相关性。L-NMMA可抑制rIL-2诱导NO的产生而添加L-Arg可逆转这一作用。rIL-2组与对照组相比线粒体活性值明显受抑（0.397±0.03比0.599±0.02，P＜0.01），而添加L-NMMA可逆转（0.536±0.03，P＜0.01）。NO产生量与线粒体活性值呈负相关（P＜0.01）。结论rIL-2刺激培养大鼠心肌细胞产生NO可抑制线粒体活性。
AIM To study the effect of human recombinant interleukin-2 (rIL-2) on nitric oxide (NO) production and on mitochondrial activity in rat cultured cardiac myocytes. METHODS rIL-2, N-monomethyl-L-arginine (L-NMMA ) and Larginine (L-Arg ) respectively or simultaneously were added to the medium in cultured rat cardiac myocytes, the NO concentration in culture media and mitochondrial activity in cardiac myocytes was measured. RESULT Incubation of cardiac myocytes for 48 h with rIL-2 caused a significant increase in NO production vs control [(85±6. 1 ) vs (10±2. 5) nmol· (106 cell)-1, P＜0.01)]. The time dependent (6 h to 48 h) and dose dependent (5 × 104 to 1 × 106 IU· L-1) accumulation of NO by rIL-2 was observed. Simultaneous incubation of rIL-2 with L-NMMA greatly inhibited rIL-2 induced NO production, whose effect was reversed by L-Arg. Mitochondrial activity was significantly inhibited by rIL-2 vs control cells (0. 397 ± 0. 03 VS 0. 599 ± 0. 02, P＜ 0. 01 ) and reversed by LNMMA (0. 536±0. 03 P＜0. 01). There was negative correlation between levels of NO production and mitochondrial activity (P＜0.01). CONCLUSION The rIL-2 stimulated NO production by cultured rat cardiac myocytes could inhibite the mitochondrial activity.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1998年第5期437-439,共3页
Chinese Pharmacological Bulletin
