Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea.
Biological Resources Research Group, Gyeongnam Department of Environment Toxicology, Chemistry, Korea Institute of Toxicology, 17 Jegok-gil, Jinju 52834, Korea.
Molecules. 2022 Jun 12;27(12):3782. doi: 10.3390/molecules27123782.
Inflammation is a severe topic in the immune system and play a role as pro-inflammatory mediators. In response to such inflammatory substances, immune cells release cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Lipopolysaccharide (LPS) is known as an endotoxin in the outer membrane of Gram-negative bacteria, and it catalyzes inflammation by stimulating the secretion of inflammatory-mediated cytokines such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) by stimulated immune cells. Among the pathways involved in inflammation, nuclear factor kappa (NF-кB) and mitogen-activated protein kinases (MAPKs) are important. NF-kB is a diploid composed of p65 and IkBα and stimulates the pro- gene. MAPKs is a family consisting of the extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and p38, JNK and p38 play a role as proinflammatory mediators. Thus, we aim to determine the scutellarein (SCU) effect on LPS stimulated RAW264.7 cells. Furthermore, since scutellarein has been shown to inhibit the SARS coronavirus helicase and has been used in Chinese medicine to treat inflammatory disorders like COVID-19, it would be required to examine scutellarein's anti-inflammatory mechanism. We identified inflammation-inducing substances using western blot with RAW264.7 cells and SCU. And we discovered that was reduced by treatment with SCU in p-p65 and p-IκBα. Also, we found that p-JNK and p-ERK were also decreased but there was no effect in p-p38. In addition, we have confirmed that the iNOS was also decreased after treatment but there is no change in the expression of COX-2. Therefore, this study shows that SCU can be used as a compound to treat inflammation.
炎症是免疫系统中的一个严重课题，作为促炎介质发挥作用。针对此类炎症物质，免疫细胞会释放肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）等细胞因子。脂多糖（LPS）是革兰氏阴性菌外膜中的一种内毒素，它通过刺激免疫细胞分泌促炎细胞因子，如环氧化酶-2（COX-2）和诱导型一氧化氮合酶（iNOS），从而引发炎症。在炎症涉及的途径中，核因子 kappa（NF-кB）和丝裂原活化蛋白激酶（MAPKs）是重要的。NF-кB 是由 p65 和 IkBα组成的二聚体，可刺激前基因。MAPKs 是由细胞外信号调节激酶（ERK）、c-Jun NH2-末端激酶（JNK）和 p38 组成的家族，JNK 和 p38 作为促炎介质发挥作用。因此，我们旨在确定白杨素（SCU）对 LPS 刺激的 RAW264.7 细胞的作用。此外，由于白杨素已被证明可抑制 SARS 冠状病毒解旋酶，并在中国医学中用于治疗 COVID-19 等炎症性疾病，因此需要研究白杨素的抗炎机制。我们使用 RAW264.7 细胞和 SCU 通过 Western blot 确定了炎症诱导物质。并且我们发现，SCU 处理可降低 p-p65 和 p-IκBα。此外，我们还发现 p-JNK 和 p-ERK 也降低了，但 p-p38 没有影响。此外，我们还证实，iNOS 经处理后也降低了，但 COX-2 的表达没有变化。因此，这项研究表明，SCU 可用作治疗炎症的化合物。
