scholarly journals The Nurr1 Activator 1,1-Bis(3′-Indolyl)-1-(p-Chlorophenyl)Methane Blocks Inflammatory Gene Expression in BV-2 Microglial Cells by Inhibiting Nuclear Factor κB

2015 ◽  
Vol 87 (6) ◽  
pp. 1021-1034 ◽  
Author(s):  
Briana R. De Miranda ◽  
Katriana A. Popichak ◽  
Sean L. Hammond ◽  
Bryce A. Jorgensen ◽  
Aaron T. Phillips ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nuclear Factor Κb ◽  
Microglial Cells ◽  
Nuclear Factor ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

scholarly journals Inhibitory Effects of Astaxanthin on CML-HSA-Induced Inflammatory and RANKL-Induced Osteoclastogenic Gene Expression in RAW 264.7 Cells

Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 54
Author(s):  
A. N. M. Mamun-Or-Rashid ◽  
Tanzima Tarannum Lucy ◽  
Masayuki Yagi ◽  
Yoshikazu Yonei
Keyword(s):  
Gene Expression ◽  
Raw 264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Marker Genes ◽  
Tartrate Resistant Acid Phosphatase ◽  
Raw 264.7 ◽  
Nuclear Factor ◽  
Activated T Cells ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

Objective: Elevated levels of serum Nε-carboxymethyllysine (CML), a well-known advanced glycation end-product (AGE), were observed in patients with inflammation or osteoporosis. Astaxanthin was reported to possess anti-inflammatory and antioxidant effects. In the present study, we investigated the effects of commercially available dietary supplement AstaReal ACTR (ASR) capsule content as astaxanthin on CML-HSA-induced inflammatory and receptor activator of nuclear factor-kappa-Β ligand (RANKL)-induced osteoclastogenic gene expression. Methods: RAW 264.7 murine macrophage cells were stimulated with CML-HSA to trigger inflammatory gene expression and treated with either a vehicle control or varied concentrations of astaxanthin. Inflammatory gene expression was measured using an enzyme-linked immunosorbent assay (ELISA) or qPCR. We triggered osteoclastogenesis using RANKL, and osteoclastogenic gene expression was measured through tartrate-resistant acid phosphatase (TRAP) activity, staining, immunofluorescence, and qPCR analyses. Results: CML-HSA showed a stimulatory effect on inflammatory gene expression, and astaxanthin reduced the expression by at least two-fold. The levels of autoinflammatory gene expression were reduced by astaxanthin. The RANKL-induced osteoclastogenesis was significantly inhibited by astaxanthin, with reductions in the activation of nuclear factor-κB (NF-κB), the expression of NFATc1 (nuclear factor of activated T cells 1), multinucleated cell formation, and the expression of mature osteoclast marker genes. Conclusion: Astaxanthin has potential as a remedy for CML-HSA-induced inflammation and RANKL-induced excessive bone loss.

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