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口服发酵野生人参通过抑制核因子κB信号通路改善葡聚糖硫酸钠诱导的急性结肠炎,并保护肠道上皮屏障。

Oral administration of fermented wild ginseng ameliorates DSS-induced acute colitis by inhibiting NF-κB signaling and protects intestinal epithelial barrier.

作者信息

Seong Myeong A, Woo Jong Kyu, Kang Ju-Hee, Jang Yeong Su, Choi Seungho, Jang Young Saeng, Lee Taek Hwan, Jung Kyung Hoon, Kang Dong Kyu, Hurh Byung Seok, Kim Dae Eung, Kim Sun Yeou, Oh Seung Hyun

机构信息

Gachon Institute of Pharmaceutical Science, Gachon University, Incheon 406-840, Korea.

Research Institute, National Cancer Center, Goyang 410-769, Korea.

出版信息

BMB Rep. 2015 Jul;48(7):419-25. doi: 10.5483/bmbrep.2015.48.7.039.

Abstract

Ginseng has been widely used for therapeutic and preventive purposes for thousands of years. However, orally administered ginseng has very low bioavailability and absorption in the intestine. Therefore, fermented ginseng was developed to enhance the beneficial effects of ginseng in the intestine. In this study, we investigated the molecular mechanisms underlying the anti-inflammatory activity of fermented wild ginseng (FWG). We found that FWG significantly alleviated the severity of colitis in a dextran sodium sulfate (DSS)-induced colitis mouse model, and decreased expression level of pro-inflammatory cytokines in colonic tissue. Moreover, we observed that FWG suppressed the infiltration of macrophages in DSS-induced colitis. FWG also attenuated the transcriptional activity of nuclear factor-κB (NF-κB) by reducing the translocation of NF-κB into the nucleus. Our data indicate that FWG contains anti-inflammatory activity via NF-κB inactivation and could be useful for treating colitis.

摘要

数千年来,人参一直被广泛用于治疗和预防目的。然而,口服人参在肠道中的生物利用度和吸收率非常低。因此,开发了发酵人参以增强人参在肠道中的有益作用。在本研究中,我们研究了发酵野生人参(FWG)抗炎活性的分子机制。我们发现,FWG显著减轻了葡聚糖硫酸钠(DSS)诱导的结肠炎小鼠模型中结肠炎的严重程度,并降低了结肠组织中促炎细胞因子的表达水平。此外,我们观察到FWG抑制了DSS诱导的结肠炎中巨噬细胞的浸润。FWG还通过减少NF-κB向细胞核的转位来减弱核因子-κB(NF-κB)的转录活性。我们的数据表明,FWG通过NF-κB失活具有抗炎活性,可用于治疗结肠炎。

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