State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Avenida da Universidade, Taipa, Macao 999078, China.
State Key Laboratory of Drug Research, & Natural Products Chemistry Department, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zu-Chong-Zhi Road, Zhangjiang Hi-Tech Park, Shanghai 201203, China.
Food Funct. 2021 Jul 20;12(14):6432-6441. doi: 10.1039/d1fo00972a.
Ten new polyisoprenylated benzophenone derivatives, 4,8-epi-uralione F (1), 4,8-epi-uralione G (2), uralione S (3), coccinone J (4), 6-epi-coccinone C (5), coccinone I (6), 36-hydroxy-guttiferone J (7), multiflorone I (8), garciniagifolone F (9) and 36-hydroxy-garciniagifolone F (10), were isolated from the fruits of Garcinia cambogia, along with seven known analogues. The structures of the new compounds were established based on the detailed analysis of 1D and 2D nuclear magnetic resonance (NMR) spectra and high resolution electrospray ionization mass spectrometra (HRESIMS), and their absolute configurations were determined from the electronic circular dichroism (ECD) spectra. All the isolates were tested for their inhibitory effects against nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. The results indicated that compound 1 displayed a potent NO inhibitory effect with an IC50 value of 41.60 ± 0.17 μM. Furthermore, compound 1 suppressed inducible NO synthase (iNOS) expression in a dose-dependent manner through inhibiting the activation of nuclear factor-κB (NF-κB).
从 Garcinia cambogia 的果实中分离得到了 10 个新的多异戊二烯基二苯甲酮衍生物，包括 4,8-epi-uralione F（1）、4,8-epi-uralione G（2）、uralione S（3）、coccinone J（4）、6-epi-coccinone C（5）、coccinone I（6）、36-羟基-乌苏烷酮 J（7）、千层酮 I（8）、garciniagifolone F（9）和 36-羟基-garciniagifolone F（10），以及 7 个已知类似物。新化合物的结构是根据 1D 和 2D 核磁共振（NMR）谱和高分辨率电喷雾电离质谱（HRESIMS）的详细分析确定的，其绝对构型是根据电子圆二色性（ECD）光谱确定的。所有分离物均测试了其对脂多糖（LPS）刺激的 RAW264.7 巨噬细胞中一氧化氮（NO）产生的抑制作用。结果表明，化合物 1 对 LPS 刺激 RAW264.7 巨噬细胞产生的一氧化氮（NO）具有很强的抑制作用，IC50 值为 41.60±0.17μM。此外，化合物 1 通过抑制核因子-κB（NF-κB）的激活，以剂量依赖的方式抑制诱导型一氧化氮合酶（iNOS）的表达。
