Table 3.
Summary of in vitro studies of anti-inflammatory activities of PCA.
| Model | Method | PCA concentration | Major finding | Interpretation | Reference |
|---|---|---|---|---|---|
| RAW 264.7 cells | Lipopolysaccharide- (LPS-) induced cellular damage | 1, 2, 5, and 25 μM | (i) PCA decreased TNF-α and IL-1β
(ii) PCA decreased NO and PGE2 (iii) PCA inhibited iNOS and COX-2 expression (iv) PCA inhibited IkB-α degradation (v) PCA inhibited NF-kB phosphorylation (vi) PCA inhibited p38, ERK, and JNK |
PCA had anti-inflammatory effects by regulating NF-kB and MAPK activation | [37] |
|
| |||||
| Mouse aortic endothelial cell (MAEC) | TNF-α-induced cellular damage | 0.05, 0.5, 5.0, 10, 20, and 40 μmol/L | (i) PCA inhibited adhesion of HL-60 cells to MAECs (ii) PCA suppressed VCAM-1 and ICAM-1 mRNA expression (iii) PCA reduced NF-kB activation |
PCA had an anti-inflammatory effect by inhibiting monocyte adhesion molecules | [38] |
|
| |||||
| Cell culture | Isolated peripheral blood monocytes (PBMs) from ApoE-deficient mice | 0.125, 0.25, and 0.5 μmol/L | (i) PCA decreased CCR2 protein and mRNA expression (ii) PCA inhibited mouse PBMs migration |
PCA exerted antiatherogenic properties by inhibiting monocyte infiltration | [39] |