Mechanism of Rehmannia glutinosa-medicated serum regulating BV2 microglia polarization to interfere with neuroinflammation
- VernacularTitle:地黄醇提物含药血清调控BV2小胶质细胞极化干预神经炎症的机制
- Author:
Ping TIAN
1
;
Hongzhi AN
1
;
Qian FEI
2
;
Ruifeng LIANG
1
;
Dan YANG
1
;
Xuexia ZHANG
1
;
Wenjing GE
1
;
Yifei LIU
1
;
Hongwei LI
2
;
Deen HAN
2
Author Information
1. Central Laboratory，Henan Integrative Medicine Hospital （Henan Academy of Chinese Medicine），Zhengzhou 450004，China
2. School of Pharmacy，Henan University of Chinese Medicine，Zhengzhou 450046，China
- Publication Type:Journal Article
- Keywords:
Rehmannia glutinosa;
medicated serum;
microglia;
neuroinflammation;
TLR4/NF-κB/NLRP3 signaling pathway;
depression
- From:
China Pharmacy
2026;37(15):1979-1985
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To study the mechanism of action of Rehmannia glutinosa-medicated serum （RG） in regulating lipopolysaccharide （LPS）-induced polarization of BV2 microglia to interfere with neuroinflammation. METHODS An in vitro neuroinflammation model of BV2 cells induced by LPS was established. Cells were divided into control group， LPS group， 10%RG group， 20%RG group， BAY 11-7082 [nuclear factor kappa B （NF-κB） inhibitor] group， and 20%RG+BAY 11-7082 group. Except for the control group， cells in all other groups were pretreated with corresponding drugs for 12 h and then stimulated with LPS for 24 h. The morphology of cells in each group was observed， and the fluorescence intensity of ionized calcium binding adaptor molecule 1 （Iba-1）， inducible nitric oxide synthase （iNOS）， CD206， the mRNA expression of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， IL-1β， iNOS， IL-4， IL-10， transforming growth factor-β （TGF-β）， arginase-1 （Arg-1）， and the Toll-like receptor 4 （TLR4）/NF-κB/NOD-like receptor thermal protein domain associated protein 3 （NLRP3） signaling pathway-related protein expression were detected. RESULTS Compared with the control group， the LPS group showed significant changes in cell morphology， exhibiting a typical M1 activated morphology. The fluorescence intensity of Iba-1 and iNOS， the relative expression levels of TNF-α， IL-6， IL-1β， iNOS mRNA， the relative expression levels of TLR4， NLRP3， caspase-1 p20， IL-1β p17 protein， and the phosphorylation levels of NF-κB p65 and inhibitor of nuclear factor kappa B α were significantly increased （P＜0.05）. The fluorescence intensity of CD206 and the relative expression levels of IL-4， IL-10， TGF-β， and Arg-1 mRNA were significantly reduced （P＜0.05）. Compared with the LPS group， the changes in the above indicators in the cells of the 10%RG group， 20%RG group， BAY 11-7082 group， and 20%RG+BAY 11-7082 group were significantly reversed （P＜0.05）， and there was no statistically significant difference in the comparison of the last three groups （P＞0.05）. CONCLUSIONS RG can effectively inhibit the overall activation of microglia and correct their M1/M2 polarization imbalance， and its mechanism may be closely related to the inhibition of excessive activation of the TLR4/NF-κB/NLRP3 signaling pathway.
