Effect of Shenlian Extract on Macrophage Function and Inflammatory Resolution in Lipid Peroxidation Inflammatory Injury Models
10.13422/j.cnki.syfjx.20191001
- VernacularTitle: 脂质过氧化炎症损伤模型中参莲提取物对巨噬细胞功能的药效与机制探讨
- Author:
Jie YIN
1
;
Qi LI
2
;
Zheng ZHAO
2
;
Qing YANG
2
;
Si-si LIU
1
;
Yu-jie LI
2
;
Ying CHEN
2
;
Ya-jie WANG
2
;
Xiao-gang WENG
2
;
Wei-yan CAI
2
;
Xiao-xin ZHU
2
Author Information
1. School of Traditional Chinese Medicine, Capital Medical University, Beijing 100069, China
2. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China
- Publication Type:Research Article
- Keywords:
lipid peroxidation inflammatory damage model;
Shenlian extract;
macrophage;
inflammation resolution;
foam;
chemotaxis
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2019;25(10):26-32
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the effect of Shenlian extract (SL extract) on macrophage function and inflammatory resolution in lipid peroxidation inflammatory injury models. Method:The effects of different concentrations of SL extract (2.5, 5.0, 10.0, 20.0 mg·L-1) on the polarization type, foam formation and chemotactic function of macrophages were detected with RAW264.7 cells induced by oxidized low-density lipoprotein(ox-LDL). Western blot was used to detect pro-inflammatory resolution factor arachidonate 5-lipoxygenase(ALOX5) and inducible inducible nitric oxide synthase(iNOS), and phosphorylated p65 (p-p65) and phosphorylated IκK (p-IκK) in nuclear factor(NF)-κB related signaling pathways. Result:Compared with the control group, ox-LDL enhanced the expressions of M1 macrophage markers TNF-α, IL-1β, iNOS (P<0.01), inhibited the expressions of IL-10 of M2 markers, promoted foam cell formation (P<0.01), induced THP-1 chemotaxis ability, increased the content of MCP-1 (P<0.01), and inhibited the expression of ALOX5.Compared with the model group, SL extract reduced the expressions of TNF-α, IL-1β, and iNOS (P<0.01), increased the expression of IL-10 (P<0.05), and down-regulated the formation of foam of macrophages (P<0.01). In transwell assay, SL extract obviously decreased the MCP-1 secretion and the number of chemotaxis cells (P<0.01), and promoted the increase of the inflammatory resolution factor ALOX5.The phosphorylation of p65 and IκK was inhibited significantly (P<0.01). Conclusion:In the inflammatory damage model of lipid peroxidation, SL extract can regulate the polarization of macrophage, inhibit the chemotaxis and foaming of ox-LDL, increase the inflammatory resolution molecular expression, and improve the state of lipid peroxidation, which may be related to the inhibition of NF-κB signaling pathway.
