Exopolysaccharide Isolated from Lactobacillus plantarum L-14 Has Anti-Inflammatory Effects via the Toll-Like Receptor 4 Pathway in LPS-Induced RAW 264.7 Cells

被引:54
作者
Kwon, Mijin [1 ]
Lee, Jaehoon [2 ]
Park, Sangkyu [1 ,2 ]
Kwon, Oh-Hee [2 ]
Seo, Jeongmin [2 ]
Roh, Sangho [1 ]
机构
[1] Seoul Natl Univ, Dent Res Inst, Cellular Reprogramming & Embryo Biotechnol Lab, Sch Dent, Seoul 08826, South Korea
[2] NeoRegen Biotech Co Ltd, Biomed Res Inst, Gyeonggi Do 16614, South Korea
基金
新加坡国家研究基金会;
关键词
postbiotics; exopolysaccharide; lipopolysaccharide; Toll-like receptor 4; inflammation; oxidative stress; TRANSCRIPTION FACTOR NRF2; INFLAMMATORY RESPONSE; ANTIOXIDATION; DISEASES;
D O I
10.3390/ijms21239283
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Inflammation is a biological response of the immune system to defend the body from negative stimulation. However, the excessive inflammatory response can damage host tissues and pose serious threats. Exopolysaccharide (EPS), one of the postbiotics, is secreted from lactic acid bacteria. Although many studies have described the beneficial effects of EPS, such as its anti-inflammatory and anti-oxidant effects, its underlying mechanisms have remained to be poorly understood. Thus, we identified that EPS obtained from Lactobacillus plantarum L-14 was a homogeneous polysaccharide primarily comprised of glucose. To examine these anti-inflammatory effects, an inflammatory response was induced by lipopolysaccharide (LPS) administration to mouse macrophage RAW 264.7 cells that were pretreated with EPS. The anti-inflammatory effects of EPS were identified by analyzing the changes within inflammatory markers at the molecular level. We demonstrate here that EPS suppressed proinflammatory mediators, such as cyclooxygenase-2, interleukin-6, tumor necrosis factor-alpha, and interleukin-1 beta, and downregulated the expression of an inducible nitric oxide synthase known to lead to oxidative stress. It was also confirmed that EPS had anti-inflammatory effects by blocking the interaction of LPS with Toll-like receptor 4 (TLR4), as demonstrated by using the known TLR4 inhibitor TAK-242. In addition, we found that EPS itself could suppress the expression of TLR4. Consequently, our data suggest that EPS can be a potential target for the development of natural product-derived medicine for treating inflammatory diseases related to TLR4.
引用
收藏
页码:1 / 18
页数:18
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