MV suppressed M1 macrophage polarization and inflammatory response, which was partially through NF-κB and p38 MAPK in LPS+IFN-γ induced BMDMs under high glucose condition, implying the potential of MV in treatment for inflammatory complications of diabetes.
Keyphrases
- high glucose
- signaling pathway
- inflammatory response
- lps induced
- endothelial cells
- oxidative stress
- pi k akt
- type diabetes
- lipopolysaccharide induced
- epithelial mesenchymal transition
- toll like receptor
- induced apoptosis
- diabetic rats
- nuclear factor
- cardiovascular disease
- dendritic cells
- immune response
- cell proliferation
- glycemic control
- anti inflammatory
- human health
- skeletal muscle