CAJ | 학술논문

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(10-4mol/L)可显著抑制巨噬细胞产生一氧化氮（NO）(P＜0.01)，较NG-硝基-左旋精氨酸（L-NNA）作用增强(P＜0.01)；且可显著减少巨噬细胞内环磷酸鸟苷（cGMP）水平(P＜0.01)，较L-NNA作用增强(P＜0.05)。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(1.5×10-4mol/L)对cNOS的抑制程度减小(P＜0.05)。活性实验结果表明：目标化合物抑制大鼠腹腔巨噬细胞内iNOS活性显著强于L-NNA，而抑制大鼠血管壁cNOS活性却弱于L-NNA。
액상합성법합성료유좌선정안산、좌선뢰안산조성적초기정안산-뢰안산삼태HCl．Arg(NO2)-Lys(OCH3)-Arg(NO2)·HCl，병연구기대원생형일양화담합매（cNOS）화유생형일양화담합매（iNOS）적억제정도。배양대서복강거서세포실험결과현시：목표화합물(10-4mol/L)가현저억제거서세포산생일양화담（NO）(P＜0.01)，교NG-초기-좌선정안산（L-NNA）작용증강(P＜0.01)；차가현저감소거서세포내배린산조감（cGMP）수평(P＜0.01)，교L-NNA작용증강(P＜0.05)。대서리체주동맥억제실험결과현시：여L-NNA상비，목표화합물(1.5×10-4mol/L)대cNOS적억제정도감소(P＜0.05)。활성실험결과표명：목표화합물억제대서복강거서세포내iNOS활성현저강우L-NNA，이억제대서혈관벽cNOS활성각약우L-NNA。
A new tripeptide HCl．Arg(NO2)-Lys(OCH3)-Arg(NO2)·HCl containingL-Arginine and L-Lysine was synthesized by the solusion phase synthesis,the inhibition of the target compound on cNOS and iNOS were studied too.Results of rat peritoneal macrophage culture were:The target compound(10-4 mol/L)could significantly inhibit macrophages to produce NO(P＜0.01),and had more potency than L-NNA(P＜0.01);it could also significantly reduce the level of cGMP in macrophages(P＜0.01),and had more potency than L-NNA(P＜0.05).Results of rat isolated aortic ring incubation was:The target compound(1.5×10-4 mol/L)played less inhibitory role in cNOS of rat aorta,compared with L-NNA(P＜0.05).It is clear by the activity experiment,that the target compound inhibits iNOS in rat peritoneal macrophages more potently than L-NNA and inhibits cNOS less potently than L-NNA.