Cao Dang Long, Woo Min-Seok, Kim Eun-Jin, Ahn Byeonggyu, Prayoga Anjas Happy, Kang Sang Soo, Cho Kye Man, Kang Dawon
Department of Physiology College of Medicine, Gyeongsang National University Jinju Republic of Korea.
Department of Convergence Medical Science Gyeongsang National University Jinju Republic of Korea.
Food Sci Nutr. 2024 Oct 18;12(11):9566-9576. doi: 10.1002/fsn3.4518. eCollection 2024 Nov.
Fermented and aged mountain-cultivated ginseng sprouts (FAMCGS) exhibit superior antioxidant and anti-inflammatory properties compared to mountain-cultivated ginseng sprouts (MCGS). However, the mechanisms behind these properties of FAMCGSE remain unclear. This study explores the anti-inflammatory effects of FAMCGS extract (FAMCGSE) on LPS-stimulated RAW 264.7 macrophages and the underlying mechanisms. The MTT assay confirmed that FAMCGSE (0 to 0.1%) maintained cell viability without inducing morphological changes. Pretreatment with FAMCGSE significantly mitigated LPS-induced morphological alterations dose-dependently. RT-PCR and Western blot analyses showed that FAMCGSE significantly reduced the mRNA and protein levels of proinflammatory mediators such as TNF-α, IL-1β, IL-6, iNOS, and COX-2. Additionally, FAMCGSE decreased the production of TNF-α, IL-1β, IL-6, nitric oxide, and PGE in LPS-activated RAW264.7 cells. Mechanistically, FAMCGSE inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs; ERK, p38, and JNK) and prevented the LPS-induced nuclear translocation of NF-κB, with effects comparable to compound K (CK) or dexamethasone. Notably, FAMCGSE was particularly effective in inhibiting ERK and JNK activation, with less impact on p38, suggesting a specific inhibitory action on certain MAPK pathways. These findings highlight FAMCGSE's potential as an inhibitor of MAPK and NF-κB pathways, indicating that FAMCGSE, including its main component CK, may be a promising therapeutic agent for inflammation-related conditions.
与山地种植人参芽(MCGS)相比,发酵陈化山地种植人参芽(FAMCGS)具有更强的抗氧化和抗炎特性。然而,FAMCGSE这些特性背后的机制仍不清楚。本研究探讨了FAMCGS提取物(FAMCGSE)对脂多糖刺激的RAW 264.7巨噬细胞的抗炎作用及其潜在机制。MTT分析证实,FAMCGSE(0至0.1%)维持细胞活力且不诱导形态变化。FAMCGSE预处理显著减轻脂多糖诱导的形态改变,呈剂量依赖性。RT-PCR和蛋白质印迹分析表明,FAMCGSE显著降低促炎介质如TNF-α、IL-1β、IL-6、诱导型一氧化氮合酶和环氧化酶-2的mRNA和蛋白质水平。此外,FAMCGSE降低了脂多糖激活的RAW264.7细胞中TNF-α、IL-1β、IL-6、一氧化氮和前列腺素E的产生。机制上,FAMCGSE抑制丝裂原活化蛋白激酶(MAPK;细胞外信号调节激酶、p38和c-Jun氨基末端激酶)的磷酸化,并阻止脂多糖诱导的核因子κB核转位,其效果与化合物K(CK)或地塞米松相当。值得注意的是,FAMCGSE在抑制细胞外信号调节激酶和c-Jun氨基末端激酶激活方面特别有效,对p38的影响较小,表明对某些MAPK途径具有特异性抑制作用。这些发现突出了FAMCGSE作为MAPK和核因子κB途径抑制剂的潜力,表明FAMCGSE及其主要成分CK可能是治疗炎症相关疾病的有前景的药物。