Department of Pharmacy, China Medical University, Taichung 404, Taiwan.
Am J Chin Med. 2014;42(6):1485-506. doi: 10.1142/S0192415X14500931.
In this study, we have investigated the anti-inflammatory effects of trilinolein (TL) using a lipopolysaccharide (LPS)-stimulated mouse macrophage (RAW264.7) and carrageenan (Carr)-induced mouse paw edema model. When RAW264.7 macrophages were treated with different concentrations of TL together with LPS, a significant concentration-dependent inhibition of nitric oxide (NO), tumor necrosis factor (TNF-α), interleukin-1 (IL-1β), and IL-6 production was detected. Western blotting revealed that TL blocked the protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-κB (NF-κB), IκBα, and mitogen-activated protein kinases (MAPKs). In the anti-inflammatory test, TL decreased the paw edema at the 5th h after λ-Carr administration in paw edema. We also demonstrated TL significantly attenuated the malondialdehyde (MDA) level in the edema paw at the 5th h after Carr injection. TL decreased the NO and TNF-α levels on the serum level at the 5th h after Carr injection. Western blotting revealed that TL decreased Carr-induced iNOS and COX-2 expressions at the 5th h in the edema paw. The anti-inflammatory mechanisms of TL might be related to the decrease in the level of iNOS, COX-2, IκBα, and MAPK pathway through the suppression of TNF-α, IL-1β, and IL-6.
在这项研究中,我们使用脂多糖 (LPS) 刺激的小鼠巨噬细胞 (RAW264.7) 和角叉菜胶 (Carr) 诱导的小鼠爪肿胀模型研究了三油精 (TL) 的抗炎作用。当 RAW264.7 巨噬细胞用不同浓度的 TL 与 LPS 一起处理时,检测到一氧化氮 (NO)、肿瘤坏死因子 (TNF-α)、白细胞介素-1 (IL-1β) 和 IL-6 产生的浓度依赖性抑制。Western blot 显示 TL 阻断了诱导型一氧化氮合酶 (iNOS)、环氧化酶-2 (COX-2)、核因子-κB (NF-κB)、IκBα 和丝裂原活化蛋白激酶 (MAPKs) 的蛋白表达。在抗炎试验中,TL 在 λ-Carr 给药后第 5 小时降低了爪肿胀。我们还表明,TL 在 Carr 注射后第 5 小时显着降低了水肿爪中的丙二醛 (MDA) 水平。TL 在 Carr 注射后第 5 小时降低了血清中 NO 和 TNF-α 的水平。Western blot 显示,TL 在水肿爪中第 5 小时降低了 Carr 诱导的 iNOS 和 COX-2 表达。TL 的抗炎机制可能与通过抑制 TNF-α、IL-1β 和 IL-6 降低 iNOS、COX-2、IκBα 和 MAPK 途径的水平有关。