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液相合成法合成了由左旋精氨酸、左旋赖氨酸组成的硝基精氨酸 赖氨酸三肽HCl·Arg(NO2 ) Lys(OCH3) Arg(NO2 )·HCl,并研究其对原生型一氧化氮合酶 (cNOS)和诱生型一氧化氮合酶 (iNOS)的抑制程度。培养大鼠腹腔巨噬细胞实验结果显示 :目标化合物 (10 -4 mol/L)可显著抑制巨噬细胞产生一氧化氮 (NO) (P <0 0 1) ,较NG 硝基 左旋精氨酸 (L NNA)作用增强 (P <0 0 1) ;且可显著减少巨噬细胞内环磷酸鸟苷 (cGMP)水平 (P <0 0 1) ,较L NNA作用增强 (P <0 0 5 )。大鼠离体主动脉抑制实验结果显示 :与L NNA相比 ,目标化合物 (1 5× 10 -4 mol/L)对cNOS的抑制程度减小 (P <0 0 5 )。活性实验结果表明 :目标化合物抑制大鼠腹腔巨噬细胞内iN OS活性显著强于L NNA ,而抑制大鼠血管壁cNOS活性却弱于L NNA。
Liquid-phase synthesis of L-arginine, L-lysine composition of arginine lysine lysine tripeptide HCl · Arg (NO2) Lys (OCH3) Arg (NO2) · HCl, and study of its original Type nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) inhibition. The results showed that the target compound (10 -4 mol / L) could significantly inhibit the production of nitric oxide (NO) in macrophages (P <0.01), which was higher than that in NG nitro-L-arginine (P <0.01). The level of cyclic guanosine monophosphate (cGMP) in macrophages (P <0.01) and the effect of LNA were enhanced (P <0 05) . The results of rat aortic intima inhibition showed that the target compound (1 5 × 10 -4 mol / L) had less cNOS inhibition than L NNA (P <0.05). The results of the activity test showed that the target compound inhibited the iNOS activity in rat peritoneal macrophages significantly stronger than LNA, while the inhibitory effect on the cNOS activity in the rat vascular wall was weaker than that of LNA.