Tang Tiantian, Wang Yujiao, Li Taotao, Liu Ding, Yang Kai, Sun Jing, Shi Yajun, Guo Dongyan, Zou Junbo, Bai Fengyun, Sun Ying, Wang Mei, Zhang Xiaofei
Key Laboratory of Basic and New Drug Research in Chinese Medicine, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, People's Republic of China.
Shaanxi Provincial University Engineering Research Center of Chinese Medicine Aromatic Industry, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, People's Republic of China.
J Inflamm Res. 2024 Aug 1;17:5139-5160. doi: 10.2147/JIR.S473596. eCollection 2024.
To explore the mechanism and active components of the anti-colitis effects of myrrh essential oil (MEO).
In this study, we investigated the anti-inflammatory effects and molecular mechanisms of MEO on dextran sulfate sodium (DSS)-induced colitis with in vitro cell experiments, RNA-seq (RNA Sequencing), Weighted gene co-expression network analysis (WGCNA), combined with "weighting coefficient" network pharmacology, as and in vivo pharmacodynamic experiments. A 3% DSS solution was used to induce colitis in BALB/c mice and MEO was administered orally. We performed gas chromatography-mass spectrometry (GC-MS) analysis of the MEO components. The disease activity index (DAI) was evaluated by observing body weight, fecal characteristics, and blood in the stool of mice. The levels of inflammatory cytokines (TNF-α and IL-1β) in mouse serum were measured using ELISA (Enzyme-linked immunosorbent assay) kits. Additionally, the expression of MAPK-related proteins (JNK, p-JNK, ERK, and p-ERK) in mouse colonic tissues was detected by Western blotting and immunohistochemistry.
MEO (0.0625-0.125µg/g, p.o). significantly inhibited the expression of the inflammatory mediator Nitric oxide (NO) in lipopolysaccharide (LPS)-induced RAW264.7 macrophages. After treatment, there was a significant increase in body weight and alleviation of diarrhea and bloody stools in colitis mice. It also reduced inflammatory cell infiltration. Furthermore, it decreased the serum levels of TNF-α and IL-1β, and reduced the activity of p-JNK and p-ERK in the MAPK pathway.
MEO relieved DSS-induced colitis by modulating the MAPK pathway. The experimental results indicate that the MAPK pathway might be inhibited by the synergistic effect of gamma-Muurolene, Curzerene, beta-Elemene, and Furanoeudesma 1.3-diene in MEO, which provides a novel idea for subsequent research and development of new anti-colitis drugs.
探讨没药精油（MEO）抗结肠炎作用的机制及活性成分。
在本研究中，我们通过体外细胞实验、RNA测序（RNA-seq）、加权基因共表达网络分析（WGCNA），结合“加权系数”网络药理学以及体内药效学实验，研究MEO对葡聚糖硫酸钠（DSS）诱导的结肠炎的抗炎作用及分子机制。用3% DSS溶液诱导BALB/c小鼠患结肠炎，并口服给予MEO。我们对MEO成分进行了气相色谱-质谱（GC-MS）分析。通过观察小鼠体重、粪便特征和粪便中的血液来评估疾病活动指数（DAI）。使用酶联免疫吸附测定（ELISA）试剂盒测量小鼠血清中炎症细胞因子（TNF-α和IL-1β）的水平。此外，通过蛋白质免疫印迹法和免疫组织化学检测小鼠结肠组织中MAPK相关蛋白（JNK、p-JNK、ERK和p-ERK）的表达。
MEO（0.0625 - 0.125μg/g，口服）显著抑制脂多糖（LPS）诱导的RAW264.7巨噬细胞中炎症介质一氧化氮（NO）的表达。治疗后，结肠炎小鼠体重显著增加，腹泻和便血症状减轻。它还减少了炎症细胞浸润。此外，它降低了血清中TNF-α和IL-1β的水平，并降低了MAPK途径中p-JNK和p-ERK的活性。
MEO通过调节MAPK途径缓解DSS诱导的结肠炎。实验结果表明，MEO中的γ-榄香烯、莪术烯、β-榄香烯和呋喃桉叶二烯1.3 - 二烯的协同作用可能抑制MAPK途径，这为后续新型抗结肠炎药物的研发提供了新思路。
