LIU Si-si, LI Qi, SUN Li-dong, et al. Effects of Shenlian Extract on Lipopolysaccharide-induced Inflammation of Macrophages[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(10): 85-91.
LIU Si-si, LI Qi, SUN Li-dong, et al. Effects of Shenlian Extract on Lipopolysaccharide-induced Inflammation of Macrophages[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(10): 85-91. DOI: 10.13422/j.cnki.syfjx.2017100085.
Objective: To investigate the therapeutic effects and mechanism of Shenlian (SL) extract on inflammatory regulation. Method: The models of inflammation based on peritoneal macrophages and Raw264.7 cells were established by being induced by lipopolysaccharides (LPS). Treatment groups were given SL extract (5
10
20 mg·L-1) for 24 h. The blank group was also set up. The protein and mRNA content of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA) and PCR (Real-time PCR); p65 in nuclear factor-κB (NF-κB) and phosphorylated p65 (p-p65) protein expression were detected by Western blot
and subcellular location of Raw264.7 cells and peritoneal macrophage NF-κB-p65 was determined by immunofluorescence. Result: Compared with the blank group
the model group showed significant increases in Raw264.7 and macrophage TNF-α
IL-1β content and mRNA expressions
Raw264.7 p-p65/p65 protein expression (P<0.01). According to the immunofluorescence assay
the model group showed obvious nuclear import of Raw264.7 cells and peritoneal macrophages. Compared with the model group
low
medium and high-dose SL extract groups showed significant decreases in Raw264.7 cells and peritoneal macrophage Raw264.7 and peritoneal macrophage TNF-α
IL-1β content and mRNA expressions(P<0.05
P<0.01)
and Raw264.7 p-p65 protein expression(P<0.01). And the medium-dose SL extract group showed an obvious weak nuclear import of Raw264.7 cells and peritoneal macrophages. Conclusion: SL extract can inhibit the inflammatory reaction of macrophages. Its mechanism may be related to the secretion of inflammatory cytokines and NF-κB signaling pathways in macrophages.