School of Basic Medical Science, Ningxia Medical University, Yinchuan 750004, P. R. China.
Food Funct. 2020 Oct 1;11(10):8537-8546. doi: 10.1039/c9fo02574j. Epub 2020 Oct 14.
This study investigated the anti-inflammatory and analgesic activities of indigo in mice and explored the possible related mechanisms. Xylene-induced ear edema, carrageenan-induced paw edema, and acetic acid-induced vascular permeability tests were used in investigating the anti-inflammatory activities. The anti-nociceptive effects of indigo were assessed through acetic acid-induced writhing, hot plate test, and formalin test, and spontaneous locomotor activity and motor performance were evaluated. The mechanisms of activities of indigo were explored by evaluating the expression levels of IκB kinase (IKK)β, p-IKKβ, inhibitor κB (IκB)α, p-IκBα, p65 nuclear factor (NF)-kB, p-p65 NF-κB, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) through western blotting and the expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and prostaglandin E (PGE) through enzyme-linked immunosorbent assay. The results showed that indigo significantly reduced xylene-induced ear edema, carrageenan-induced paw edema, and acetic acid-induced vascular permeation. In addition, indigo significantly inhibited nociception induced by acetic acid and formalin. However, the level of nociception was not decreased by indigo in the hot plate test, and indigo did not affect spontaneous locomotor activity and motor performance. The expression levels of p-IKKβ, p-IκBα, p65 NF-kB, p-p65 NF-κB, COX-2, iNOS, TNF-α, IL-1β, IL-6, and PGE decreased, whereas the expression level of IκBα increased obviously after indigo treatment. In conclusion, indigo exerts significant anti-inflammatory and analgesic activities in mice by inhibiting IKKβ phosphorylation and reducing the production of important pain mediators, such as PGE and COX-2, via the IKKβ/IκB/NF-κB pathway.
本研究旨在探讨青黛的抗炎和镇痛活性，并探讨其可能的相关机制。采用二甲苯诱导的耳肿胀、角叉菜胶诱导的足肿胀和醋酸诱导的血管通透性试验来研究青黛的抗炎活性。通过醋酸诱导的扭体、热板试验和福尔马林试验评估青黛的镇痛作用，并评估自发运动活动和运动表现。通过评估 IκB 激酶 (IKK)β、p-IKKβ、抑制κB (IκB)α、p-IκBα、p65 核因子 (NF)-κB、p-p65 NF-κB、环加氧酶-2 (COX-2) 和诱导型一氧化氮合酶 (iNOS) 的表达水平，探讨青黛活性的机制，通过蛋白质印迹法和肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β)、白细胞介素-6 (IL-6) 和前列腺素 E (PGE) 的表达水平，通过酶联免疫吸附试验。结果表明，青黛显著减轻二甲苯诱导的耳肿胀、角叉菜胶诱导的足肿胀和醋酸诱导的血管通透性。此外，青黛显著抑制醋酸和福尔马林诱导的疼痛。然而，青黛并未降低热板试验中疼痛的程度，并且青黛不影响自发运动活动和运动表现。p-IKKβ、p-IκBα、p65 NF-κB、p-p65 NF-κB、COX-2、iNOS、TNF-α、IL-1β、IL-6 和 PGE 的表达水平明显降低，而 IκBα 的表达水平明显增加。综上所述，青黛通过抑制 IKKβ 磷酸化并通过 IKKβ/IκB/NF-κB 途径减少重要疼痛介质（如 PGE 和 COX-2）的产生，在小鼠中发挥显著的抗炎和镇痛作用。
