WANG Bo, YU Shan, HE Jiang-bo, et al. Effect of Ursolic Acid on Cholesterol Efflux and PPAR- Gene and Protein Expression in RAW264.7 Macrophage-derived Foam Cells[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(10): 127-132.
WANG Bo, YU Shan, HE Jiang-bo, et al. Effect of Ursolic Acid on Cholesterol Efflux and PPAR- Gene and Protein Expression in RAW264.7 Macrophage-derived Foam Cells[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(10): 127-132. DOI: 10.13422/j.cnki.syfjx.2017100127.
Objective: To observe the effects of different concentrations of ursolic acid (UA) on cholesterol efflux and peroxisome proliferatros activated receptor -γ (PPAR-γ) transporter expression in RAW264.7 macrophage-derived foam cells
and its possible mechanism. Method: RAW264.7 macrophages were cultured in vitro and incubated with 20 mg·L-1 oxidized low density lipoprotein (ox-LDL) for 48 hours to induce foam cells. Oil red O staining was used to identify morphological changes of foam cells. The mRNA and protein expressions of PPAR-γ were detected by Real-time polyerse chinrection (PCR) and enzyme-linked immunosorbent assay (ELISA). Result: Macrophages were transformed into foam cells by being induced with ox-LDL for 48 h. Compared with the blank group
the cholesterol efflux rate of foamed cells in the UA intervention group increased at concentrations of 10
15
20
25 mg·L-1(P<0.01)
and were dose-dependently within a certain concentration range. At concentrations of 10
15
20
25 mg·L-1
the protein expression of PPAR-γ mRNA in foam cells in the UA intervention group was up-regulated(P<0.01)
and wasdose-dependently within a certain concentration range. The protein expression of PPAR-γ in foam cells of UA treated at concentrations of 10
15
20
25 mg·L-1 increased (P<0.01)
and the difference was statistically significant. Conclusion: After 20 mg·L-1ox-LDL induced macrophages are differentiated into foam cells
a large number of intracellular lipid increases
and UA promotes macrophage cholesterol efflux
which may be related to increase in intracellular expression of PPAR-γ.