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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。
Objective To investigate the effects of human recombinant interleukin-2 (IL-2) on the production of nitric oxide (NO) and mitochondrial activity in cultured rat cardiomyocytes. Methods The rIL-2, monomethyl L-arginine (L-NMMA) and L-arginine (L-arginine) were added respectively or simultaneously in the culture of cardiomyocytes. Mitochondrial activity values. Results Compared with the control group, NO production increased significantly (48 ± 6.1) and (10 ± 2.5) nmol · (106 cells) -1, P <0.01, respectively. The correlation between rIL-2-stimulated NO production time (6 ~ 48h) and dose (5 × 104 ~ 1 × 106IU · L-1) L-NMMA can inhibit the production of NO induced by rIL-2 and L-Arg can reverse this effect. Compared with the control group, the mitochondrial activity of rIL-2 group was significantly inhibited (0.397 ± 0.03 vs 0.599 ± 0.02, P <0.01), while the addition of L-NMMA reversed (0.536 ± 0.03, P <0.01). NO production and mitochondrial activity was negatively correlated (P <0.01). Conclusion RIL-2 stimulates the cultured rat cardiomyocytes to produce NO and inhibits mitochondrial activity.