FOOD SCIENCE ›› 2021, Vol. 42 ›› Issue (5): 129-136.doi: 10.7506/spkx1002-6630-20200105-043

• Nutrition & Hygiene • Previous Articles     Next Articles

Protective Effect of Lyophyllum ulmarium Fibrinolytic Enzyme on Endothelial Cells from Injury Induced by Lipopolysaccharide

GENG Chao, WEI Ying, SHEN Minghua   

  1. (Medical College, Yanbian University, Yanji 133002, China)
  • Online:2021-03-15 Published:2021-03-29

Abstract: Objective: To investigate the protective effect of Lyophyllum ulmarium fibrinolytic enzyme (LUFE) on inflammatory injury induced by lipopolysaccharide (LPS) in vascular endothelial cells. Methods: An in vitro inflammation model was created by stimulating human umbilical vein endothelial cells (HUVEC) with LPS. The HUVEC were divided into five groups including control, model and low-, medium- and high-dose LUFE groups. The survival rate of HUVEC was determined by MTT assay. The levels of lactate dehydrogenase (LDH) activity, tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), E-selectin and monocyte chemoattractant protein 1 (MCP-1) in the cell culture supernatant were investigated by enzyme-linked immunosorbent assay (ELISA). The Hoechst method was adopted to observe the adhesion between HUVEC and human acute monocytic leukemia cell line-1 (THP-1). The expression of intercellular cell adhesion molecule 1 (ICAM1) in HUVEC was detected by flow cytometry. Western blot assay was used to detect the expression and activation of toll-like receptor 4 (TLR4), mitogen-activated protein kinase (MAPK) and the major proteins involved in the nuclear factor κB (NF-κB) signaling pathway including myeloid differentiation factor 88 (MyD88), transforming growth factor β activated kinase 1 (TAK1) and phosphorylated TAK1 (p-TAK1). Results: LUFE inhibited the LPS-induced increase in the levels of LDH, TNF-α, IL-6, E-selectin and MCP-1 in the culture supernatant of HUVEC, decreased the expression level of ICAM-1, and reduced the adhesion of HUVEC to THP-1. Compared with the model group, the levels of TLR4 and MyD88, p-TAK1/TAK1 ratio, the ratio of phosphorylated c-Jun N-terminal kinase (p-JNK) to JNK, the ratio of phosphorylated protein-38 (p-p38) to p38, and the ratio of phosphorylated NF-κB (p-NF-κB) to NF-κB in all three LUFE treatment groups were significantly reduced (P < 0.05). Conclusion: LUFE has a protective effect on inflammatory injury in HUVEC, and its underlying mechanism may be though inhibiting the TLR4/MyD88/TAK1/NF-κB signaling pathway and the MAPK signaling pathway and thereby reducing the level of inflammatory factors.

Key words: Lyophyllum ulmarium fibrinolytic enzyme; lipopolysaccharide; endothelial cell; inflammation

CLC Number: