Ju Hye Kyung, Baek Suk-Hwan, An Ren-Bo, Bae KiHwan, Son Kun Ho, Kim Hyun Pyo, Kang Sam Sik, Lee Sung Ho, Son Jong Keun, Chang Hyeun Wook
College of Pharmacy, Yeungnam University, Gyongsan, Korea.
Biol Pharm Bull. 2003 Oct;26(10):1375-8. doi: 10.1248/bpb.26.1375.
Nardostachin, which is an iridoid isolated from Patrinia saniculaefolia, was examined by assessing its effect on the production of tumor necrosis factor-alpha (TNF-alpha) and expression of 2 enzymes, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in lipopolysaccharide (LPS)-stimulated Raw264.7 macrophages. This compound consistently inhibited the production of nitric oxide (NO) and TNF-alpha production in a dose-dependent manner, with respective IC(50) values of 12.3 and 16.2 microM. The decrease in quantity of NO products was accompanied by a decrease in the iNOS protein level, as assessed by Western blotting probed with specific anti-iNOS antibodies. In addition, this compound also reduced the COX-2 protein expression level and the attendant PGE(2) production in LPS-stimulated macrophages. These results suggest that nardostachin may be useful for inhibiting the production of inflammatory mediators such as TNF-alpha, NO and PGE(2) in inflammatory diseases.
从山地糙苏中分离得到的环烯醚萜类化合物甘松新酮，通过评估其对脂多糖（LPS）刺激的Raw264.7巨噬细胞中肿瘤坏死因子-α（TNF-α）产生以及两种酶（诱导型一氧化氮合酶（iNOS）和环氧合酶-2（COX-2））表达的影响进行了研究。该化合物以剂量依赖性方式持续抑制一氧化氮（NO）的产生和TNF-α的产生，其半数抑制浓度（IC50）分别为12.3和16.2微摩尔。如用特异性抗iNOS抗体进行蛋白质印迹法评估所示，NO产物量的减少伴随着iNOS蛋白水平的降低。此外，该化合物还降低了LPS刺激的巨噬细胞中COX-2蛋白表达水平以及随之而来的前列腺素E2（PGE2）的产生。这些结果表明，甘松新酮可能有助于抑制炎症性疾病中TNF-α、NO和PGE2等炎症介质的产生。
